The Experts below are selected from a list of 12264 Experts worldwide ranked by ideXlab platform
Jae Jun Song - One of the best experts on this subject based on the ideXlab platform.
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the luxs ai 2 quorum sensing system of streptococcus pneumoniae is required to cause disease and to regulate virulence and metabolism related genes in a rat model of middle Ear Infection
Frontiers in Cellular and Infection Microbiology, 2018Co-Authors: Mukesh Kumar Yadav, Jorge E Vidal, Shin H Kim, Sung Won Chae, Jae Jun SongAbstract:Objective:Streptococcus pneumoniae colonizes the nasopharynx of children, and from nasopharynx it could migrate to the middle Ear and causes acute otitis media (AOM). During colonization and AOM, the pneumococcus forms biofilms. In vitro biofilm formation requires a functional LuxS/AI-2 quorum-sensing system. We investigated the role of LuxS/AI-2 signaling in pneumococcal middle Ear Infection, and identified the genes that are regulated by LuxS/AI-2 during pneumococcal biofilm formation. Methods:Streptococcus pneumoniae D39 wild-type and an isogenic D39ΔluxS strain were utilized to evaluate in vitro biofilm formation, and in vivo colonization and epithelial damage using a microtiter plate assay and a rat model of pneumococcal middle Ear Infection, respectively. Biofilm structures and colonization and epithelial damage were evaluated at the ultrastructural level by scanning electron microscopy and confocal microscopy. Microarrays were used to investigate the global genes that were regulated by LuxS/AI-2 during biofilm formation. Results: The biofilm biomass and density of D39ΔluxS were significantly (p < 0.05) lower than those of D39 wild-type. SEM and confocal microscopy revealed that D39ΔluxS formed thin biofilms in vitro compared with D39 wild-type. The in vivo model of middle Ear Infection showed that D39ΔluxS resulted in ~60% less (p < 0.05) bacterial colonization than the wild-type. SEM analysis of the rat middle Ears revealed dense biofilm-like cell debris deposited on the cilia in wild-type D39-infected rats. However, little cell debris was deposited in the middle Ears of the D39ΔluxS-inoculated rats, and the cilia were visible. cDNA-microarray analysis revealed 117 differentially expressed genes in D39ΔluxS compared with D39 wild-type. Among the 66 genes encoding putative proteins and previously characterized proteins, 60 were significantly downregulated, whereas 6 were upregulated. Functional annotation revealed that genes involved in DNA replication and repair, ATP synthesis, capsule biosynthesis, cell division, the cell cycle, signal transduction, transcription regulation, competence, virulence, and carbohydrate metabolism were downregulated in the absence of LuxS/AI-2. Conclusion: The S. pneumoniae LuxS/AI-2 quorum-sensing system is necessary for biofilm formation and the colonization of the Ear epithelium, and caused middle Ear Infection in the rat model. LuxS/AI-2 regulates the expression of the genes involved in virulence and bacterial fitness during pneumococcal biofilm formation.
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the luxs ai 2 quorum sensing system of streptococcus pneumoniae is required to cause disease and to regulate virulence and metabolism related genes in a rat model of middle Ear Infection
Frontiers in Cellular and Infection Microbiology, 2018Co-Authors: Mukesh Kumar Yadav, Jorge E Vidal, Sung Won Chae, Yoon Young Go, Jae Jun SongAbstract:Objective: Streptococcus pneumoniae colonizes the nasopharynx of children, and from nasopharynx it could migrate to the middle Ear and causes acute otitis media (AOM). During colonization and AOM, the pneumococcus forms biofilms. In vitro biofilm formation requires a functional LuxS/AI-2 quorum-sensing system. We investigated the role of LuxS/AI-2 signaling in pneumococcal middle Ear Infection, and identified the genes that are regulated by LuxS/AI-2 during pneumococcal biofilm formation. Methods: S. pneumoniae D39 wild-type and an isogenic D39luxS strain were utilized to evaluate in vitro biofilm formation, and in vivo colonization and epithelial damage using a microtiter plate assay and a rat model of pneumococcal middle Ear Infection, respectively. Biofilm structures and colonization and epithelial damage were evaluated at the ultrastructural level by scanning electron microscopy and confocal microscopy. Microarrays were used to investigate the global genes that were regulated by LuxS/AI-2 during biofilm formation. Results: The biofilm biomass and density of D39luxS were significantly (p < 0.05) lower than those of D39 wild-type. SEM and confocal microscopy revealed that D39luxS formed thin biofilms in vitro compared with D39 wild-type. The in vivo model of middle Ear Infection showed that D39luxS resulted in 60% less (p < 0.05) bacterial colonization than the wild-type. SEM analysis of the rat middle Ears revealed dense biofilm-like cell debris deposited on the cilia in wild-type D39-infected rats. However, little cell debris was deposited in the middle Ears of the D39luxS-inoculated rats, and the cilia were visible. cDNA-microarray analysis revealed 117 differentially expressed genes in D39luxS compared with D39 wild-type. Among the 66 genes encoding putative proteins and previously characterized proteins, 60 were significantly downregulated, whereas 6 were upregulated. Functional annotation revealed that genes involved in DNA replication and repair, ATP synthesis, capsule biosynthesis, cell division, the cell cycle, signal transduction, transcription regulation, competence, virulence, and carbohydrate metabolism were downregulated in the absence of LuxS/AI-2. Conclusion: The S. pneumoniae LuxS/AI-2 quorum-sensing system is necessary for biofilm formation and the colonization of the Ear epithelium, and caused middle Ear Infection in the rat model. LuxS/AI-2 regulates the expression of the genes involved in virulence and bacterial fitness during
Stephane F Maison - One of the best experts on this subject based on the ideXlab platform.
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mice lacking adrenergic signaling have normal cochlEar responses and normal resistance to acoustic injury but enhanced susceptibility to middle Ear Infection
Jaro-journal of The Association for Research in Otolaryngology, 2010Co-Authors: Stephane F Maison, Mina Le, Erik Larsen, John J Rosowski, Steven A ThomasAbstract:The vasculature and neurons of the inner Ear receive adrenergic innervation from the cervical sympathetic chain, and adrenergic receptors may be expressed by cells of the organ of Corti and stria vascularis, despite a lack of direct sympathetic innervation. To assess the functional role of adrenergic signaling in the auditory periphery, we studied mice with targeted deletion of the gene for dopamine β-hydroxylase (DBH), which catalyzes the conversion of dopamine to noradrenaline; thus, these mutant mice have no measurable adrenaline or noradrenaline. Dbh−/− mice were more susceptible to spontaneous middle-Ear Infection than their control littermates, consistent with a role for sympathetics in systemic and/or local immune response. At 6–8 weeks of age, cochlEar thresholds and suprathreshold responses assessed by auditory brainstem responses and distortion product otoacoustic emissions, as well as light-microscopic morphology, were indistinguishable from controls, if Ears with conductive hEaring loss were eliminated. Dbh−/− mice were no more susceptible to acoustic injury than controls, despite prior reports that sympathectomy reduces noise damage. Dbh−/− mice showed enhancement of shock-evoked olivocochlEar suppression of cochlEar responses, which may arise from the loss of adrenergic inputs to olivocochlEar neurons in the brainstem. However, adrenergic modulation of olivocochlEar efferents does not mediate the protective effect of contralateral cochlEar destruction on ipsilateral response to acoustic overexposure.
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mice lacking adrenergic signaling have normal cochlEar responses and normal resistance to acoustic injury but enhanced susceptibility to middle Ear Infection
Jaro-journal of The Association for Research in Otolaryngology, 2010Co-Authors: Stephane F Maison, Erik Larsen, John J Rosowski, Suhkyung Lee, Steven A ThomasAbstract:The vasculature and neurons of the inner Ear receive adrenergic innervation from the cervical sympathetic chain, and adrenergic receptors may be expressed by cells of the organ of Corti and stria vascularis, despite a lack of direct sympathetic innervation. To assess the functional role of adrenergic signaling in the auditory periphery, we studied mice with targeted deletion of the gene for dopamine beta-hydroxylase (DBH), which catalyzes the conversion of dopamine to noradrenaline; thus, these mutant mice have no measurable adrenaline or noradrenaline. Dbh (-/-) mice were more susceptible to spontaneous middle-Ear Infection than their control littermates, consistent with a role for sympathetics in systemic and/or local immune response. At 6-8 weeks of age, cochlEar thresholds and suprathreshold responses assessed by auditory brainstem responses and distortion product otoacoustic emissions, as well as light-microscopic morphology, were indistinguishable from controls, if Ears with conductive hEaring loss were eliminated. Dbh (-/-) mice were no more susceptible to acoustic injury than controls, despite prior reports that sympathectomy reduces noise damage. Dbh (-/-) mice showed enhancement of shock-evoked olivocochlEar suppression of cochlEar responses, which may arise from the loss of adrenergic inputs to olivocochlEar neurons in the brainstem. However, adrenergic modulation of olivocochlEar efferents does not mediate the protective effect of contralateral cochlEar destruction on ipsilateral response to acoustic overexposure.
Mukesh Kumar Yadav - One of the best experts on this subject based on the ideXlab platform.
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the luxs ai 2 quorum sensing system of streptococcus pneumoniae is required to cause disease and to regulate virulence and metabolism related genes in a rat model of middle Ear Infection
Frontiers in Cellular and Infection Microbiology, 2018Co-Authors: Mukesh Kumar Yadav, Jorge E Vidal, Shin H Kim, Sung Won Chae, Jae Jun SongAbstract:Objective:Streptococcus pneumoniae colonizes the nasopharynx of children, and from nasopharynx it could migrate to the middle Ear and causes acute otitis media (AOM). During colonization and AOM, the pneumococcus forms biofilms. In vitro biofilm formation requires a functional LuxS/AI-2 quorum-sensing system. We investigated the role of LuxS/AI-2 signaling in pneumococcal middle Ear Infection, and identified the genes that are regulated by LuxS/AI-2 during pneumococcal biofilm formation. Methods:Streptococcus pneumoniae D39 wild-type and an isogenic D39ΔluxS strain were utilized to evaluate in vitro biofilm formation, and in vivo colonization and epithelial damage using a microtiter plate assay and a rat model of pneumococcal middle Ear Infection, respectively. Biofilm structures and colonization and epithelial damage were evaluated at the ultrastructural level by scanning electron microscopy and confocal microscopy. Microarrays were used to investigate the global genes that were regulated by LuxS/AI-2 during biofilm formation. Results: The biofilm biomass and density of D39ΔluxS were significantly (p < 0.05) lower than those of D39 wild-type. SEM and confocal microscopy revealed that D39ΔluxS formed thin biofilms in vitro compared with D39 wild-type. The in vivo model of middle Ear Infection showed that D39ΔluxS resulted in ~60% less (p < 0.05) bacterial colonization than the wild-type. SEM analysis of the rat middle Ears revealed dense biofilm-like cell debris deposited on the cilia in wild-type D39-infected rats. However, little cell debris was deposited in the middle Ears of the D39ΔluxS-inoculated rats, and the cilia were visible. cDNA-microarray analysis revealed 117 differentially expressed genes in D39ΔluxS compared with D39 wild-type. Among the 66 genes encoding putative proteins and previously characterized proteins, 60 were significantly downregulated, whereas 6 were upregulated. Functional annotation revealed that genes involved in DNA replication and repair, ATP synthesis, capsule biosynthesis, cell division, the cell cycle, signal transduction, transcription regulation, competence, virulence, and carbohydrate metabolism were downregulated in the absence of LuxS/AI-2. Conclusion: The S. pneumoniae LuxS/AI-2 quorum-sensing system is necessary for biofilm formation and the colonization of the Ear epithelium, and caused middle Ear Infection in the rat model. LuxS/AI-2 regulates the expression of the genes involved in virulence and bacterial fitness during pneumococcal biofilm formation.
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the luxs ai 2 quorum sensing system of streptococcus pneumoniae is required to cause disease and to regulate virulence and metabolism related genes in a rat model of middle Ear Infection
Frontiers in Cellular and Infection Microbiology, 2018Co-Authors: Mukesh Kumar Yadav, Jorge E Vidal, Sung Won Chae, Yoon Young Go, Jae Jun SongAbstract:Objective: Streptococcus pneumoniae colonizes the nasopharynx of children, and from nasopharynx it could migrate to the middle Ear and causes acute otitis media (AOM). During colonization and AOM, the pneumococcus forms biofilms. In vitro biofilm formation requires a functional LuxS/AI-2 quorum-sensing system. We investigated the role of LuxS/AI-2 signaling in pneumococcal middle Ear Infection, and identified the genes that are regulated by LuxS/AI-2 during pneumococcal biofilm formation. Methods: S. pneumoniae D39 wild-type and an isogenic D39luxS strain were utilized to evaluate in vitro biofilm formation, and in vivo colonization and epithelial damage using a microtiter plate assay and a rat model of pneumococcal middle Ear Infection, respectively. Biofilm structures and colonization and epithelial damage were evaluated at the ultrastructural level by scanning electron microscopy and confocal microscopy. Microarrays were used to investigate the global genes that were regulated by LuxS/AI-2 during biofilm formation. Results: The biofilm biomass and density of D39luxS were significantly (p < 0.05) lower than those of D39 wild-type. SEM and confocal microscopy revealed that D39luxS formed thin biofilms in vitro compared with D39 wild-type. The in vivo model of middle Ear Infection showed that D39luxS resulted in 60% less (p < 0.05) bacterial colonization than the wild-type. SEM analysis of the rat middle Ears revealed dense biofilm-like cell debris deposited on the cilia in wild-type D39-infected rats. However, little cell debris was deposited in the middle Ears of the D39luxS-inoculated rats, and the cilia were visible. cDNA-microarray analysis revealed 117 differentially expressed genes in D39luxS compared with D39 wild-type. Among the 66 genes encoding putative proteins and previously characterized proteins, 60 were significantly downregulated, whereas 6 were upregulated. Functional annotation revealed that genes involved in DNA replication and repair, ATP synthesis, capsule biosynthesis, cell division, the cell cycle, signal transduction, transcription regulation, competence, virulence, and carbohydrate metabolism were downregulated in the absence of LuxS/AI-2. Conclusion: The S. pneumoniae LuxS/AI-2 quorum-sensing system is necessary for biofilm formation and the colonization of the Ear epithelium, and caused middle Ear Infection in the rat model. LuxS/AI-2 regulates the expression of the genes involved in virulence and bacterial fitness during
John J Rosowski - One of the best experts on this subject based on the ideXlab platform.
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mice lacking adrenergic signaling have normal cochlEar responses and normal resistance to acoustic injury but enhanced susceptibility to middle Ear Infection
Jaro-journal of The Association for Research in Otolaryngology, 2010Co-Authors: Stephane F Maison, Mina Le, Erik Larsen, John J Rosowski, Steven A ThomasAbstract:The vasculature and neurons of the inner Ear receive adrenergic innervation from the cervical sympathetic chain, and adrenergic receptors may be expressed by cells of the organ of Corti and stria vascularis, despite a lack of direct sympathetic innervation. To assess the functional role of adrenergic signaling in the auditory periphery, we studied mice with targeted deletion of the gene for dopamine β-hydroxylase (DBH), which catalyzes the conversion of dopamine to noradrenaline; thus, these mutant mice have no measurable adrenaline or noradrenaline. Dbh−/− mice were more susceptible to spontaneous middle-Ear Infection than their control littermates, consistent with a role for sympathetics in systemic and/or local immune response. At 6–8 weeks of age, cochlEar thresholds and suprathreshold responses assessed by auditory brainstem responses and distortion product otoacoustic emissions, as well as light-microscopic morphology, were indistinguishable from controls, if Ears with conductive hEaring loss were eliminated. Dbh−/− mice were no more susceptible to acoustic injury than controls, despite prior reports that sympathectomy reduces noise damage. Dbh−/− mice showed enhancement of shock-evoked olivocochlEar suppression of cochlEar responses, which may arise from the loss of adrenergic inputs to olivocochlEar neurons in the brainstem. However, adrenergic modulation of olivocochlEar efferents does not mediate the protective effect of contralateral cochlEar destruction on ipsilateral response to acoustic overexposure.
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mice lacking adrenergic signaling have normal cochlEar responses and normal resistance to acoustic injury but enhanced susceptibility to middle Ear Infection
Jaro-journal of The Association for Research in Otolaryngology, 2010Co-Authors: Stephane F Maison, Erik Larsen, John J Rosowski, Suhkyung Lee, Steven A ThomasAbstract:The vasculature and neurons of the inner Ear receive adrenergic innervation from the cervical sympathetic chain, and adrenergic receptors may be expressed by cells of the organ of Corti and stria vascularis, despite a lack of direct sympathetic innervation. To assess the functional role of adrenergic signaling in the auditory periphery, we studied mice with targeted deletion of the gene for dopamine beta-hydroxylase (DBH), which catalyzes the conversion of dopamine to noradrenaline; thus, these mutant mice have no measurable adrenaline or noradrenaline. Dbh (-/-) mice were more susceptible to spontaneous middle-Ear Infection than their control littermates, consistent with a role for sympathetics in systemic and/or local immune response. At 6-8 weeks of age, cochlEar thresholds and suprathreshold responses assessed by auditory brainstem responses and distortion product otoacoustic emissions, as well as light-microscopic morphology, were indistinguishable from controls, if Ears with conductive hEaring loss were eliminated. Dbh (-/-) mice were no more susceptible to acoustic injury than controls, despite prior reports that sympathectomy reduces noise damage. Dbh (-/-) mice showed enhancement of shock-evoked olivocochlEar suppression of cochlEar responses, which may arise from the loss of adrenergic inputs to olivocochlEar neurons in the brainstem. However, adrenergic modulation of olivocochlEar efferents does not mediate the protective effect of contralateral cochlEar destruction on ipsilateral response to acoustic overexposure.
Anthony Hogan - One of the best experts on this subject based on the ideXlab platform.
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Ear Infection and its associated risk factors comorbidity and health service use in australian children
International Journal of Pediatrics, 2013Co-Authors: Vasoontara Yiengprugsawan, Anthony HoganAbstract:This study investigates and identifies risk factors, comorbidity, and health service use related to Ear Infection in Australian children. Two cross-sectional analyses of the Longitudinal Study of Australian Children (LSAC) involved 4,983 children aged 4 to 5 yEars in 2004 and aged 10 to 11 yEars in 2010. Odds ratios (ORs) were analysed using bivariate logistic regression. The prevalence of parent-reported Ear Infection was 7.9% (394) among children aged 4 to 5 yEars and 3.3% (139) at 10 to 11 yEars. Our study found that risk factors associated with Ear Infection were indigenous status, not being breastfed, mother or father smoking at least once a day, and father’s school completion at yEar 9 or lower. By age 10 to 11 yEars significantly reported comorbidities were tonsillitis (OR 4.67; ), headache (OR 2.13; ), and asthma (OR 1.67; ) and Ear Infection was found to be associated with the use of pediatrician (OR 1.83; ), other specialist (OR 2.12; ), and Early intervention services (OR 3.08; ). This empirical evidence can be used to inform the development of intervention and management programs for Ear Infection.
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longitudinal analysis of Ear Infection and hEaring impairment findings from 6 yEar prospective cohorts of australian children
BMC Pediatrics, 2013Co-Authors: Vasoontara Yiengprugsawan, Anthony Hogan, Lyndall StrazdinsAbstract:Middle Ear Infection is common in childhood. Despite its prevalence, there is little longitudinal evidence about the impact of Ear Infection, particularly its association to hEaring loss. By using 6-yEar prospective data, we investigate the onset and impact over time of Ear Infection in Australian children. We analyse 4 waves of the Longitudinal Study of Australian Children (LSAC) survey collected in 2004, 2006, 2008, and 2010. There are two age cohorts in this study (B cohort aged 0/1 to 6/7 yEars N=4242 and K cohort aged 4/5 to 10/11 yEars N=4169). Exposure was parent-reported Ear Infection and outcome was parent-reported hEaring problems. We modelled Ear Infection onset and subsequent impact on hEaring using multivariate logistic regressions, reporting Adjusted Odds Ratios (AOR) and Confidence Intervals (95% CI). Separate analyses were reported for indigenous and non-indigenous children. Associations of Ear Infections between waves were found to be very strong both among both indigenous and non-indigenous children in the two cohorts. Reported Ear Infections at Earlier wave were also associated with hEaring problems in subsequent wave. For example, reported Ear Infections at age 4/5 yEars among the K cohort were found to be predictors of hEaring problems at age 8/9 yEars (AOR 4.0, 95% CI 2.2-7.3 among non-indigenous children and AOR 7.7 95% CI 1.0-59.4 among indigenous children). Number of repeated Ear Infections during the 6-yEar follow-up revealed strong dose–response relationships with subsequent hEaring problems among non-indigenous children (AORs ranged from 4.4 to 31.7 in the B cohort and 4.4 to 51.0 in the K cohort) but not statistically significant among indigenous children partly due to small sample. This study revealed the longitudinal impact of Ear Infections on hEaring problems in both indigenous and non-indigenous children. These findings highlight the need for special attention and follow-up on children with repeated Ear Infections.
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Ear Infection and its associated risk factors comorbidity and health service use in australian children
Social Science Research Network, 2013Co-Authors: Vasoontara Yiengprugsawan, Anthony HoganAbstract:This study investigates and identifies risk factors, comorbidity, and health service use related to Ear Infection in Australian children. Two cross-sectional analyses of the Longitudinal Study of Australian Children (LSAC) involved 4,983 children aged 4 to 5 yEars in 2004 and aged 10 to 11 yEars in 2010. Odds ratios (ORs) were analysed using bivariate logistic regression. The prevalence of parent-reported Ear Infection was 7.9% (394) among children aged 4 to 5 yEars and 3.3% (139) at 10 to 11 yEars. Our study found that risk factors associated with Ear Infection were indigenous status, not being breastfed, mother or father smoking at least once a day, and father's school completion at yEar 9 or lower. By age 10 to 11 yEars significantly reported comorbidities were tonsillitis (OR 4.67; P
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longitudinal analysis of Ear Infection and hEaring impairment findings from 6 yEar prospective cohorts of australian
Social Science Research Network, 2013Co-Authors: Vasoontara Yiengprugsawan, Anthony Hogan, Lyndall StrazdinsAbstract:Background: Middle Ear Infection is common in childhood. Despite its prevalence, there is little longitudinal evidence about the impact of Ear Infection, particularly its association to hEaring loss. By using 6-yEar prospective data, we investigate the onset and impact over time of Ear Infection in Australian children. Methods: We analyse 4 waves of the Longitudinal Study of Australian Children (LSAC) survey collected in 2004, 2006, 2008, and 2010. There are two age cohorts in this study (B cohort aged 0/1 to 6/7 yEars N=4242 and K cohort aged 4/5 to 10/11 yEars N=4169). Exposure was parent-reported Ear Infection and outcome was parent-reported hEaring problems. We modelled Ear Infection onset and subsequent impact on hEaring using multivariate logistic regressions, reporting Adjusted Odds Ratios (AOR) and Confidence Intervals (95% CI). Separate analyses were reported for indigenous and non-indigenous children. Results: Associations of Ear Infections between waves were found to be very strong both among both indigenous and non-indigenous children in the two cohorts. Reported Ear Infections at Earlier wave were also associated with hEaring problems in subsequent wave. For example, reported Ear Infections at age 4/5 yEars among the K cohort were found to be predictors of hEaring problems at age 8/9 yEars (AOR 4.0, 95% CI 2.2-7.3 among non-indigenous children and AOR 7.7 95% CI 1.0-59.4 among indigenous children). Number of repeated Ear Infections during the 6-yEar follow-up revealed strong dose-response relationships with subsequent hEaring problems among non-indigenous children (AORs ranged from 4.4 to 31.7 in the B cohort and 4.4 to 51.0 in the K cohort) but not statistically significant among indigenous children partly due to small sample. Conclusions: This study revealed the longitudinal impact of Ear Infections on hEaring problems in both indigenous and non-indigenous children. These findings highlight the need for special attention and follow-up on children with repeated Ear Infections.