The Experts below are selected from a list of 300 Experts worldwide ranked by ideXlab platform
Joanna Floros - One of the best experts on this subject based on the ideXlab platform.
-
Gonadal hormones and oxidative stress interaction differentially affects survival of male and female mice after lung Klebsiella Pneumoniae Infection
Experimental lung research, 2012Co-Authors: Faryal Durrani, Anatoly N. Mikerov, David S. Phelps, Judith Weisz, Patricia Silveyra, Joanna FlorosAbstract:Survival of mice after Klebsiella Pneumoniae Infection and phagocytosis by alveolar macrophages (AMs), in the presence or absence of ozone (O(3)) exposure prior to Infection, is sex dependent. The objective of this work was to study the role of gonadal hormones, 5α-dihydrotestosterone (DHT) and 17β-estradiol (E(2)), on mouse survival after filtered air (FA) or O(3) exposure. Gonadectomized female (G×F) and male (G×M) mice implanted with control or hormone pellets (DHT in G×F, or E(2) in G×M), exposed to O(3) (2 ppm, 3h) or FA, and infected with K. Pneumoniae were monitored for survival. Survival in G×F was identical after FA or O(3) exposure; in G×M O(3) exposure resulted in lower survival compared to FA. In O(3)-exposed females, gonadectomy resulted in increased survival compared to intact females or to G×M+E(2). A similar effect was observed in G×F+DHT. The combined negative effect of oxidative stress and hormone on survival was higher for E(2). Gonadectomy eliminated (females) or minimized (males) the previously observed sex differences in survival in response to oxidative stress, and hormone treatment restored them. These findings indicate that gonadal hormones and/or oxidative stress have a significant effect on mouse survival.
-
Differences in the BAL proteome after Klebsiella Pneumoniae Infection in wild type and SP-A-/- mice
Proteome Science, 2010Co-Authors: Todd M Umstead, Anatoly N. Mikerov, Rizwanul Haque, Joanna Floros, Willard M Freeman, David S. PhelpsAbstract:Background Surfactant protein-A (SP-A) has been shown to play a variety of roles related to lung host defense function. Mice lacking SP-A are more susceptible to Infection than wild type C57BL/6 mice. We studied bronchoalveolar lavage (BAL) protein expression in wild type and SP-A-/- mice infected with Klebsiella Pneumoniae by 2D-DIGE. Methods Mice were infected intratracheally with K. Pneumoniae and after 4 and 24 hours they were subject to BAL. Cell-free BAL was analyzed by 2D-DIGE on two-dimensional gels with pH ranges of 4-7 and 7-11. Under baseline conditions and at 4 and 24 hr post-Infection BAL was compared between untreated and infected wild type and SP-A-/- mice. Sixty proteins identified by mass spectrometry were categorized as host defense, redox regulation, and protein metabolism/modification. Results We found: 1) ~75% of 32 host defense proteins were lower in uninfected SP-A-/- vs wild type, suggesting increased susceptibility to Infection or oxidative injury; 2) At 4 hr post-Infection > 2/3 of identified proteins were higher in SP-A-/- than wild type mice, almost the exact opposite of untreated mice; 3) At 24 hr post-Infection some proteins continued increasing, but many returned to baseline; 4) In infected wild type mice significant changes occurred in 13 of 60 proteins, with 12 of 13 increasing, vs on 4 significant changes in SP-A-/- mice. Infection response patterns between strains demonstrated both commonalities and differences. In several cases changes between 4 and 24 hr followed different patterns between strains. Conclusions These indicate that SP-A plays a key role in regulating the BAL proteome, functioning indirectly to regulate lung host defense function, possibly via the macrophage. In the absence of SP-A baseline levels of many host defense molecules are lower. However, many of these indirect deficits in SP-A-/- mice are rapidly compensated for during Infection, indicating that SP-A also has a direct role on host defense against K. Pneumoniae that may be instrumental in determining clinical course.
-
Ablation of SP-A has a negative impact on the susceptibility of mice to Klebsiella Pneumoniae Infection after ozone exposure: sex differences
Respiratory research, 2008Co-Authors: Anatoly N. Mikerov, Rizwanul Haque, Xiaozhuang Gan, Xiaoxuan Guo, David S. Phelps, Joanna FlorosAbstract:Background Surfactant protein A (SP-A) enhances phagocytosis of bacteria, including Klebsiella Pneumoniae, by alveolar macrophages. Ozone, a major air pollutant, can cause oxidation of surfactant and may influence lung immune function. Immune function may also be affected by sex-specific mechanisms. We hypothesized that ablation of SP-A has a negative impact on the susceptibility of mice to Klebsiella Pneumoniae Infection after ozone exposure, and that sex differences in the effect of ozone do exist.
-
sex differences in the impact of ozone on survival and alveolar macrophage function of mice after Klebsiella Pneumoniae Infection
Respiratory Research, 2008Co-Authors: Anatoly N. Mikerov, Xiaozhuang Gan, David S. Phelps, Todd M Umstead, Laura Miller, Vernon M Chinchilli, Joanna FlorosAbstract:Sex differences have been described in a number of pulmonary diseases. However, the impact of ozone exposure followed by pneumonia Infection on sex-related survival and macrophage function have not been reported. The purpose of this study was to determine whether ozone exposure differentially affects: 1) survival of male and female mice infected with Klebsiella Pneumoniae, and 2) the phagocytic ability of macrophages from these mice. Male and female C57BL/6 mice were exposed to O3 or to filtered air (FA) (control) and then infected intratracheally with K. Pneumoniae bacteria. Survival was monitored over a 14-day period, and the ability of alveolar macrophages to phagocytize the pathogen in vivo was investigated after 1 h. 1) Both male and female mice exposed to O3 are significantly more susceptible to K. Pneumoniae Infection than mice treated with FA; 2) although females appeared to be more resistant to K. Pneumoniae than males, O3 exposure significantly increased the susceptibility of females to K. Pneumoniae Infection to a greater degree than males; 3) alveolar macrophages from O3-exposed male and female mice have impaired phagocytic ability compared to macrophages from FA-exposed mice; and 4) the O3-dependent reduction in phagocytic ability is greater in female mice. O3 exposure reduces the ability of mice to survive K. Pneumoniae Infection and the reduced phagocytic ability of alveolar macrophages may be one of the contributing factors. Both events are significantly more pronounced in female mice following exposure to the environmental pollutant, ozone.
David S. Phelps - One of the best experts on this subject based on the ideXlab platform.
-
Gonadal hormones and oxidative stress interaction differentially affects survival of male and female mice after lung Klebsiella Pneumoniae Infection
Experimental lung research, 2012Co-Authors: Faryal Durrani, Anatoly N. Mikerov, David S. Phelps, Judith Weisz, Patricia Silveyra, Joanna FlorosAbstract:Survival of mice after Klebsiella Pneumoniae Infection and phagocytosis by alveolar macrophages (AMs), in the presence or absence of ozone (O(3)) exposure prior to Infection, is sex dependent. The objective of this work was to study the role of gonadal hormones, 5α-dihydrotestosterone (DHT) and 17β-estradiol (E(2)), on mouse survival after filtered air (FA) or O(3) exposure. Gonadectomized female (G×F) and male (G×M) mice implanted with control or hormone pellets (DHT in G×F, or E(2) in G×M), exposed to O(3) (2 ppm, 3h) or FA, and infected with K. Pneumoniae were monitored for survival. Survival in G×F was identical after FA or O(3) exposure; in G×M O(3) exposure resulted in lower survival compared to FA. In O(3)-exposed females, gonadectomy resulted in increased survival compared to intact females or to G×M+E(2). A similar effect was observed in G×F+DHT. The combined negative effect of oxidative stress and hormone on survival was higher for E(2). Gonadectomy eliminated (females) or minimized (males) the previously observed sex differences in survival in response to oxidative stress, and hormone treatment restored them. These findings indicate that gonadal hormones and/or oxidative stress have a significant effect on mouse survival.
-
Differences in the BAL proteome after Klebsiella Pneumoniae Infection in wild type and SP-A-/- mice
Proteome Science, 2010Co-Authors: Todd M Umstead, Anatoly N. Mikerov, Rizwanul Haque, Joanna Floros, Willard M Freeman, David S. PhelpsAbstract:Background Surfactant protein-A (SP-A) has been shown to play a variety of roles related to lung host defense function. Mice lacking SP-A are more susceptible to Infection than wild type C57BL/6 mice. We studied bronchoalveolar lavage (BAL) protein expression in wild type and SP-A-/- mice infected with Klebsiella Pneumoniae by 2D-DIGE. Methods Mice were infected intratracheally with K. Pneumoniae and after 4 and 24 hours they were subject to BAL. Cell-free BAL was analyzed by 2D-DIGE on two-dimensional gels with pH ranges of 4-7 and 7-11. Under baseline conditions and at 4 and 24 hr post-Infection BAL was compared between untreated and infected wild type and SP-A-/- mice. Sixty proteins identified by mass spectrometry were categorized as host defense, redox regulation, and protein metabolism/modification. Results We found: 1) ~75% of 32 host defense proteins were lower in uninfected SP-A-/- vs wild type, suggesting increased susceptibility to Infection or oxidative injury; 2) At 4 hr post-Infection > 2/3 of identified proteins were higher in SP-A-/- than wild type mice, almost the exact opposite of untreated mice; 3) At 24 hr post-Infection some proteins continued increasing, but many returned to baseline; 4) In infected wild type mice significant changes occurred in 13 of 60 proteins, with 12 of 13 increasing, vs on 4 significant changes in SP-A-/- mice. Infection response patterns between strains demonstrated both commonalities and differences. In several cases changes between 4 and 24 hr followed different patterns between strains. Conclusions These indicate that SP-A plays a key role in regulating the BAL proteome, functioning indirectly to regulate lung host defense function, possibly via the macrophage. In the absence of SP-A baseline levels of many host defense molecules are lower. However, many of these indirect deficits in SP-A-/- mice are rapidly compensated for during Infection, indicating that SP-A also has a direct role on host defense against K. Pneumoniae that may be instrumental in determining clinical course.
-
Ablation of SP-A has a negative impact on the susceptibility of mice to Klebsiella Pneumoniae Infection after ozone exposure: sex differences
Respiratory research, 2008Co-Authors: Anatoly N. Mikerov, Rizwanul Haque, Xiaozhuang Gan, Xiaoxuan Guo, David S. Phelps, Joanna FlorosAbstract:Background Surfactant protein A (SP-A) enhances phagocytosis of bacteria, including Klebsiella Pneumoniae, by alveolar macrophages. Ozone, a major air pollutant, can cause oxidation of surfactant and may influence lung immune function. Immune function may also be affected by sex-specific mechanisms. We hypothesized that ablation of SP-A has a negative impact on the susceptibility of mice to Klebsiella Pneumoniae Infection after ozone exposure, and that sex differences in the effect of ozone do exist.
-
sex differences in the impact of ozone on survival and alveolar macrophage function of mice after Klebsiella Pneumoniae Infection
Respiratory Research, 2008Co-Authors: Anatoly N. Mikerov, Xiaozhuang Gan, David S. Phelps, Todd M Umstead, Laura Miller, Vernon M Chinchilli, Joanna FlorosAbstract:Sex differences have been described in a number of pulmonary diseases. However, the impact of ozone exposure followed by pneumonia Infection on sex-related survival and macrophage function have not been reported. The purpose of this study was to determine whether ozone exposure differentially affects: 1) survival of male and female mice infected with Klebsiella Pneumoniae, and 2) the phagocytic ability of macrophages from these mice. Male and female C57BL/6 mice were exposed to O3 or to filtered air (FA) (control) and then infected intratracheally with K. Pneumoniae bacteria. Survival was monitored over a 14-day period, and the ability of alveolar macrophages to phagocytize the pathogen in vivo was investigated after 1 h. 1) Both male and female mice exposed to O3 are significantly more susceptible to K. Pneumoniae Infection than mice treated with FA; 2) although females appeared to be more resistant to K. Pneumoniae than males, O3 exposure significantly increased the susceptibility of females to K. Pneumoniae Infection to a greater degree than males; 3) alveolar macrophages from O3-exposed male and female mice have impaired phagocytic ability compared to macrophages from FA-exposed mice; and 4) the O3-dependent reduction in phagocytic ability is greater in female mice. O3 exposure reduces the ability of mice to survive K. Pneumoniae Infection and the reduced phagocytic ability of alveolar macrophages may be one of the contributing factors. Both events are significantly more pronounced in female mice following exposure to the environmental pollutant, ozone.
Anatoly N. Mikerov - One of the best experts on this subject based on the ideXlab platform.
-
Gonadal hormones and oxidative stress interaction differentially affects survival of male and female mice after lung Klebsiella Pneumoniae Infection
Experimental lung research, 2012Co-Authors: Faryal Durrani, Anatoly N. Mikerov, David S. Phelps, Judith Weisz, Patricia Silveyra, Joanna FlorosAbstract:Survival of mice after Klebsiella Pneumoniae Infection and phagocytosis by alveolar macrophages (AMs), in the presence or absence of ozone (O(3)) exposure prior to Infection, is sex dependent. The objective of this work was to study the role of gonadal hormones, 5α-dihydrotestosterone (DHT) and 17β-estradiol (E(2)), on mouse survival after filtered air (FA) or O(3) exposure. Gonadectomized female (G×F) and male (G×M) mice implanted with control or hormone pellets (DHT in G×F, or E(2) in G×M), exposed to O(3) (2 ppm, 3h) or FA, and infected with K. Pneumoniae were monitored for survival. Survival in G×F was identical after FA or O(3) exposure; in G×M O(3) exposure resulted in lower survival compared to FA. In O(3)-exposed females, gonadectomy resulted in increased survival compared to intact females or to G×M+E(2). A similar effect was observed in G×F+DHT. The combined negative effect of oxidative stress and hormone on survival was higher for E(2). Gonadectomy eliminated (females) or minimized (males) the previously observed sex differences in survival in response to oxidative stress, and hormone treatment restored them. These findings indicate that gonadal hormones and/or oxidative stress have a significant effect on mouse survival.
-
Differences in the BAL proteome after Klebsiella Pneumoniae Infection in wild type and SP-A-/- mice
Proteome Science, 2010Co-Authors: Todd M Umstead, Anatoly N. Mikerov, Rizwanul Haque, Joanna Floros, Willard M Freeman, David S. PhelpsAbstract:Background Surfactant protein-A (SP-A) has been shown to play a variety of roles related to lung host defense function. Mice lacking SP-A are more susceptible to Infection than wild type C57BL/6 mice. We studied bronchoalveolar lavage (BAL) protein expression in wild type and SP-A-/- mice infected with Klebsiella Pneumoniae by 2D-DIGE. Methods Mice were infected intratracheally with K. Pneumoniae and after 4 and 24 hours they were subject to BAL. Cell-free BAL was analyzed by 2D-DIGE on two-dimensional gels with pH ranges of 4-7 and 7-11. Under baseline conditions and at 4 and 24 hr post-Infection BAL was compared between untreated and infected wild type and SP-A-/- mice. Sixty proteins identified by mass spectrometry were categorized as host defense, redox regulation, and protein metabolism/modification. Results We found: 1) ~75% of 32 host defense proteins were lower in uninfected SP-A-/- vs wild type, suggesting increased susceptibility to Infection or oxidative injury; 2) At 4 hr post-Infection > 2/3 of identified proteins were higher in SP-A-/- than wild type mice, almost the exact opposite of untreated mice; 3) At 24 hr post-Infection some proteins continued increasing, but many returned to baseline; 4) In infected wild type mice significant changes occurred in 13 of 60 proteins, with 12 of 13 increasing, vs on 4 significant changes in SP-A-/- mice. Infection response patterns between strains demonstrated both commonalities and differences. In several cases changes between 4 and 24 hr followed different patterns between strains. Conclusions These indicate that SP-A plays a key role in regulating the BAL proteome, functioning indirectly to regulate lung host defense function, possibly via the macrophage. In the absence of SP-A baseline levels of many host defense molecules are lower. However, many of these indirect deficits in SP-A-/- mice are rapidly compensated for during Infection, indicating that SP-A also has a direct role on host defense against K. Pneumoniae that may be instrumental in determining clinical course.
-
Ablation of SP-A has a negative impact on the susceptibility of mice to Klebsiella Pneumoniae Infection after ozone exposure: sex differences
Respiratory research, 2008Co-Authors: Anatoly N. Mikerov, Rizwanul Haque, Xiaozhuang Gan, Xiaoxuan Guo, David S. Phelps, Joanna FlorosAbstract:Background Surfactant protein A (SP-A) enhances phagocytosis of bacteria, including Klebsiella Pneumoniae, by alveolar macrophages. Ozone, a major air pollutant, can cause oxidation of surfactant and may influence lung immune function. Immune function may also be affected by sex-specific mechanisms. We hypothesized that ablation of SP-A has a negative impact on the susceptibility of mice to Klebsiella Pneumoniae Infection after ozone exposure, and that sex differences in the effect of ozone do exist.
-
sex differences in the impact of ozone on survival and alveolar macrophage function of mice after Klebsiella Pneumoniae Infection
Respiratory Research, 2008Co-Authors: Anatoly N. Mikerov, Xiaozhuang Gan, David S. Phelps, Todd M Umstead, Laura Miller, Vernon M Chinchilli, Joanna FlorosAbstract:Sex differences have been described in a number of pulmonary diseases. However, the impact of ozone exposure followed by pneumonia Infection on sex-related survival and macrophage function have not been reported. The purpose of this study was to determine whether ozone exposure differentially affects: 1) survival of male and female mice infected with Klebsiella Pneumoniae, and 2) the phagocytic ability of macrophages from these mice. Male and female C57BL/6 mice were exposed to O3 or to filtered air (FA) (control) and then infected intratracheally with K. Pneumoniae bacteria. Survival was monitored over a 14-day period, and the ability of alveolar macrophages to phagocytize the pathogen in vivo was investigated after 1 h. 1) Both male and female mice exposed to O3 are significantly more susceptible to K. Pneumoniae Infection than mice treated with FA; 2) although females appeared to be more resistant to K. Pneumoniae than males, O3 exposure significantly increased the susceptibility of females to K. Pneumoniae Infection to a greater degree than males; 3) alveolar macrophages from O3-exposed male and female mice have impaired phagocytic ability compared to macrophages from FA-exposed mice; and 4) the O3-dependent reduction in phagocytic ability is greater in female mice. O3 exposure reduces the ability of mice to survive K. Pneumoniae Infection and the reduced phagocytic ability of alveolar macrophages may be one of the contributing factors. Both events are significantly more pronounced in female mice following exposure to the environmental pollutant, ozone.
David P Calfee - One of the best experts on this subject based on the ideXlab platform.
-
decreased susceptibility to polymyxin b during treatment for carbapenem resistant Klebsiella Pneumoniae Infection
Journal of Clinical Microbiology, 2009Co-Authors: Jooyun Lee, David P Calfee, Shirish Huprikar, Gopi Patel, Stephen G JenkinsAbstract:In the United States, the major mechanism of carbapenem resistance among Enterobacteriaceae is the production of Klebsiella Pneumoniae carbapenemase (KPC) (2). Polymyxins and tigecycline are the antimicrobials most often used for treatment of Infections caused by carbapenem-resistant Enterobacteriaceae (4, 11). Polymyxin B, discovered more than 60 years ago, has been reintroduced as a valuable therapeutic agent with efficacy against multidrug-resistant gram-negative bacteria due to a shortage of new antimicrobials with activities against these organisms. While polymyxin B resistance has been observed in clinical isolates of carbapenem-resistant K. Pneumoniae (CRKP), reports of developing resistance in vivo during treatment with polymyxin B are limited (1, 8). We studied patients with CRKP Infections who persistently had positive cultures despite ≥3 days of treatment with either polymyxin B alone or polymyxin B and tigecycline. The patients were hospitalized between July 2004 and June 2006 at the Mount Sinai Hospital (New York, NY). The history of antibiotic therapy and the duration of treatment were obtained from patients' medical records and hospital pharmacy records. Carbapenem resistance in K. Pneumoniae isolates was initially detected by using an automated broth microdilution system (MicroScan; Dade Behring, Deerfield, IL), followed by confirmation with the disk diffusion assay and Etest (AB Biodisk, Solna, Sweden). The presence of the KPC gene in each isolate was tested by PCR analysis using primers and conditions described elsewhere (12). The MICs for polymyxin B and tigecycline were determined by Etest. Of the 16 patients included in this study, 12 received polymyxin B (polymyxin B sulfate) alone for a mean duration of 12.6 days (range, 3 to 25 days) and 4 received both polymyxin B and tigecycline for a mean duration of 9.3 days (range, 4 to 23 days) and 9 days (range, 3 to 16 days), respectively. Polymyxin B and tigecycline were given as a combination therapy for a mean duration of 6.25 days (range, 3 to 15 days) for those who received both agents. All patients received a therapeutic dose of polymyxin B, which was renally adjusted if needed. The initial CRKP isolates were recovered from blood (12 patients), peritoneal fluid (2 patients), sputum (1 patient), and cerebrospinal fluid (1 patient) samples. All of the subsequent CRKP isolates were recovered from blood samples. The KPC gene was present in all initial and subsequent isolates as confirmed by PCR analysis. The mean time interval between the recovery of initial and subsequent isolates was 16.6 days (range, 4 to 55 days) for those who received polymyxin B alone and 15.5 days (range, 4 to 42 days) for those who received both polymyxin B and tigecycline. Significant increases in the polymyxin B MIC were observed in the subsequent isolates recovered from 3 of 12 patients (25%) treated with only polymyxin B: 1.5 μg/ml to 32 μg/ml, 0.75 μg/ml to 12 μg/ml, and 0.75 μg/ml to 1024 μg/ml, respectively (Table (Table1).1). The mean durations of treatment with polymyxin B for these three patients were not different from those for the other nine patients whose subsequent isolates did not have an increased MIC (mean, 15.7 days versus 10.8 days; P = 0.46). During the study period, more than 90% of CRKP clinical isolates at our institution demonstrated in vitro susceptibilities to polymyxin B. None of the subsequent isolates from patients who received both polymyxin B and tigecycline showed changes in the MIC for either polymyxin B or tigecycline. TABLE 1. Increased MIC of polymyxin B for CRKP isolates from three patients treated with polymyxin B This observation may be explained by the emergence of resistance in the same strain or reInfection with a resistant strain from a heterogeneous bacterial population under antibiotic selective pressure. The clonal relationship between the initial and subsequent isolates was not examined in this study. The mechanisms of resistance to polymyxin in K. Pneumoniae may be mediated by modification of the lipopolysaccharide of the outer membrane or by increased production of capsular polysaccharide (5, 13). These molecular changes induced by mutation are known to confer a low level of resistance and occur slowly (3, 5), in contrast to our cases in which isolates showed a significantly increased MIC in a relatively short period of time: 14 days, 21 days, and 5 days, respectively (Table (Table1).1). ReInfection with a resistant strain under antibiotic selective pressure might be implicated in these cases, and perhaps combination therapy with polymyxin B and tigecycline might have prevented this in patients who received both agents. Although polymyxin and tigecycline do not show a synergistic effect on K. Pneumoniae in vitro (10), they are not antagonistic and may have an additive effect when used together (9). Of importance is that combination therapy may prevent the emergence of resistance in CRKP isolates. Further studies are needed to determine the clinical significance of our findings and to evaluate the in vivo efficacy of combination therapy with polymyxin and tigecycline for treatment of CRKP Infection.
-
outcomes of carbapenem resistant Klebsiella Pneumoniae Infection and the impact of antimicrobial and adjunctive therapies
Infection Control and Hospital Epidemiology, 2008Co-Authors: Gopi Patel, Shirish Huprikar, Stephen G Jenkins, David P CalfeeAbstract:Background. Carbapenem‐resistant Klebsiella Pneumoniae is an emerging healthcare‐associated pathogen. Objective. To describe the epidemiology of and clinical outcomes associated with carbapenem‐resistant K. Pneumoniae Infection and to identify risk factors associated with mortality among patients with this type of Infection. Setting. Mount Sinai Hospital, a 1,171‐bed tertiary care teaching hospital in New York City. Design. Two matched case‐control studies. Methods. In the first matched case‐control study, case patients with carbapenem‐resistant K. Pneumoniae Infection were compared with control patients with carbapenem‐susceptible K. Pneumoniae Infection. In the second case‐control study, patients who survived carbapenem‐resistant K. Pneumoniae Infection were compared with those who did not survive, to identify risk factors associated with mortality among patients with carbapenem‐resistant K. Pneumoniae Infection. Results. There were 99 case patients and 99 control patients identified. Carbapenem‐resista...
Virginia L. Miller - One of the best experts on this subject based on the ideXlab platform.
-
Comparison of the Host Responses to Wild-Type and cpsB Mutant Klebsiella Pneumoniae Infections
Infection and immunity, 2006Co-Authors: Matthew S. Lawlor, Scott A. Handley, Virginia L. MillerAbstract:Previously, we established an intranasal mouse model of Klebsiella Pneumoniae Infection and validated its utility using a highly virulent wild-type strain and an avirulent capsular polysaccharide mutant. In the present study we compare the host responses to both Infections by examining cytokine production, cellular infiltration, pulmonary histology, and intranasal immunization.