Inefficiency of C3H/HeN mice to control chlamydial lung infection correlates with downregulation of neutrophil activation during the late stage of infection.
We previously reported that massive infiltration of neutrophils in C3H/HeN (C3H) mice could not efficiently control Chlamydia muridarum (Cm) infection and might contribute to the high susceptibility of these mice to lung infection. To further define the nature of neutrophil responses in C3H mice during chlamydial infection, we examine the expression of adhesion molecules and CD11b related to neutrophils infiltration and activation, respectively, following intranasal Cm infection. The results showed that the expression of selectins (E-selectin, P-selectin and L-selectin), and intercellular cell adhesion molecule-1 (ICAM-1) in the lung of C3H mice increased more significantly than in C57BL/6 (B6) mice, the more resistant strain. These results correlated well with the massive neutrophils infiltration in C3H mice. In contrast, CD11b expression on peripheral blood and lung neutrophils in C3H mice exhibited a significant reduction compared with B6 mice during the late phage of infection (day 14). These findings suggest that the high-level expression of adhesion molecules in C3H mice may enhance neutrophils recruitment to the lung, but the decline of CD11b expression on neutrophils may attenuate neutrophil function. Therefore, CD11b down-regulation on neutrophils may contribute to the failure of C3H mice to control chlamydial lung infection.
Tang
Xiaofei
X
Department of Immunology, Tianjin Medical University, Tianjin Key Laboratory of Cellular and Molecular Immunology, Key Laboratory of Educational Ministry of China, Tianjin, China.
Bu
Xiaokun
X
Zhang
Naihong
N
Li
Xiaoxia
X
Huang
Huanjun
H
Bai
Hong
H
Yang
Xi
X
D000818:Animals; D039481:CD11b Antigen / Q000096:biosynthesis / Q000235:genetics; D002690:Chlamydia Infections / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D023502:Chlamydia muridarum / Q000276:immunology*; D020022:Genetic Predisposition to Disease; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D008168:Lung / Q000473:pathology; D051379:Mice; D008809:Mice, Inbred C3H; D008810:Mice, Inbred C57BL; D018375:Neutrophil Activation; D020556:Neutrophil Infiltration; D009504:Neutrophils / Q000276:immunology / Q000378:metabolism* / Q000382:microbiology / Q000473:pathology; D018410:Pneumonia, Bacterial / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D019087:Selectins / Q000235:genetics / Q000276:immunology / Q000378:metabolism*
D039481:CD11b Antigen; D019087:Selectins; D018799:Intercellular Adhesion Molecule-1