tetano
Editor, Senior Moderator
Microb Pathog. 2018 Dec 5;127:212-219. doi: 10.1016/j.micpath.2018.12.008. [Epub ahead of print]
[h=1]Macrophage CD14 impacts immune defenses against influenza virus in allergic hosts.[/h] Palipane M[SUP]1[/SUP], Snyder JD[SUP]2[/SUP], LeMessurier KS[SUP]1[/SUP], Schofield AK[SUP]3[/SUP], Woolard SN[SUP]4[/SUP], Samarasinghe AE[SUP]5[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Asthma and influenza are leading causes of worldwide morbidity and mortality. Although these two conditions can co-exist in the same patient, the immune parameters that impact disease outcomes are not fully elucidated. The importance of macrophages to both conditions suggested a role for CD14, a co-receptor for endotoxin, as a regulatory mechanism for innate immune responses during asthma and influenza co-morbidity. Herein, we hypothesized that parameters of influenza morbidity will be reduced in the absence of CD14. Age and gender matched wild-type (WT) and CD14 knock-out (KO) mice were subjected to our validated model of Aspergillus-induced model of asthma and/or influenza. Characteristics of disease pathogenesis were investigated using standard methods in weight loss, flow cytometry, airway resistance, histology, quantitative real-time PCR, and viral titer quantification. The absence of CD14 did not have an impact on morbidity as these mice were equally susceptible to disease with similar airway resistance. Peribronchovascular inflammation and goblet cell content were equivalent between WT and KO mice in asthma alone and asthma and influenza co-morbidity. Co-morbid KO mice had less lymphocytes and eosinophils in the airways although their lung viral burden was equivalent to WT. Inflammatory gene signatures were altered in co-morbid mice in each genotype. CD14 expression on macrophages is necessary for airway inflammation but not for viral pathogenesis in allergic hosts.
[h=4]KEYWORDS:[/h] Fungal asthma; Inflammation; Mouse
PMID: 30529429 DOI: 10.1016/j.micpath.2018.12.008
[h=1]Macrophage CD14 impacts immune defenses against influenza virus in allergic hosts.[/h] Palipane M[SUP]1[/SUP], Snyder JD[SUP]2[/SUP], LeMessurier KS[SUP]1[/SUP], Schofield AK[SUP]3[/SUP], Woolard SN[SUP]4[/SUP], Samarasinghe AE[SUP]5[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Asthma and influenza are leading causes of worldwide morbidity and mortality. Although these two conditions can co-exist in the same patient, the immune parameters that impact disease outcomes are not fully elucidated. The importance of macrophages to both conditions suggested a role for CD14, a co-receptor for endotoxin, as a regulatory mechanism for innate immune responses during asthma and influenza co-morbidity. Herein, we hypothesized that parameters of influenza morbidity will be reduced in the absence of CD14. Age and gender matched wild-type (WT) and CD14 knock-out (KO) mice were subjected to our validated model of Aspergillus-induced model of asthma and/or influenza. Characteristics of disease pathogenesis were investigated using standard methods in weight loss, flow cytometry, airway resistance, histology, quantitative real-time PCR, and viral titer quantification. The absence of CD14 did not have an impact on morbidity as these mice were equally susceptible to disease with similar airway resistance. Peribronchovascular inflammation and goblet cell content were equivalent between WT and KO mice in asthma alone and asthma and influenza co-morbidity. Co-morbid KO mice had less lymphocytes and eosinophils in the airways although their lung viral burden was equivalent to WT. Inflammatory gene signatures were altered in co-morbid mice in each genotype. CD14 expression on macrophages is necessary for airway inflammation but not for viral pathogenesis in allergic hosts.
[h=4]KEYWORDS:[/h] Fungal asthma; Inflammation; Mouse
PMID: 30529429 DOI: 10.1016/j.micpath.2018.12.008