Open AccessThe B ordetella pertussis B ps polysaccharide enhances lung colonization by conferring protection from complement‐mediated killing
Author(s) -
Ganguly Tridib,
Johnson John B.,
Kock Nancy D.,
Parks Griffith D.,
Deora Rajendar
Publication year - 2014
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/cmi.12264
Subject(s) - bordetella pertussis , biology , complement system , microbiology and biotechnology , alternative complement pathway , factor h , classical complement pathway , whooping cough , mutant , pertussis toxin , bordetella , flow cytometry , complement membrane attack complex , innate immune system , immune system , virology , immunology , bacteria , gene , receptor , genetics , g protein , vaccination
Summary B ordetella pertussis is a human‐restricted G ram‐negative bacterial pathogen that causes whooping cough or pertussis. Pertussis is the leading vaccine preventable disease that is resurging in the USA and other parts of the developed world. There is an incomplete understanding of the mechanisms by which B . pertussis evades killing and clearance by the complement system, a first line of host innate immune defence. The present study examined the role of the B ps polysaccharide to resist complement activity in vitro and in the mouse respiratory tract. The isogenic bps mutant strain containing a large non‐polar in‐frame deletion of the bpsA–D locus was more sensitive to serum and complement mediated killing than the WT strain. As determined by W estern blotting, flow cytometry and electron microscopic studies, the heightened sensitivity of the mutant strain was due to enhanced deposition of complement proteins and the formation of membrane attack complex, the end‐product of complement activation. B ps was sufficient to confer complement resistance as evidenced by a B ps‐expressing E scherichia coli being protected by serum killing. Additionally, W estern blotting and flow cytometry assays revealed that B ps inhibited the deposition of complement proteins independent of other B . pertussis factors. The bps mutant strain colonized the lungs of complement‐deficient mice at higher levels than that observed in C 57 B l/6 mice. These results reveal a previously unknown interaction between B ps and the complement system in controlling B . pertussis colonization of the respiratory tract. These findings also make B ps a potential target for the prevention and therapy of whooping cough.