Role of neutrophils in controlling early stages of a Chlamydia trachomatis infection. Infect. Immun

Inoculation of mice with the granulocyte-depleting monoclonal antibody RB6-8C5 showed that neutrophils are critical protective effector cells during a Chlamydia trachomatis infection. In addition, administration of monoclonal antibody 2E6 demonstrated that extravasation of neutrophils into the peritoneal cavity in response to inoculation with the C. trachomatis MoPn biovar is dependent on the surface b-2 integrin molecule CD18. Chlamydia trachomatis is a gram-negative obligate intracel-lular bacterium that can infect a wide range of hosts and cause a variety of diseases in humans including sexually transmitted diseases and trachoma (3, 15, 26). Neutrophils are the most predominant effector cells recruited to the infectious foci dur-ing the early stages of a chlamydial infection (1, 4, 19, 20, 27). In spite of this, the role of neutrophils in a chlamydial infection is not clearly understood (13, 28, 29). With the advent of monoclonal antibodies (MAb), the possibility of assessing the functional role of neutrophils in vivo has now become feasible. Here, we utilized two MAb, RB6-8C5 and 2E6, to determine the role that neutrophils may have during a chlamydial infec-tion. RB6-8C5 is a rat immunoglobulin G2b (IgG2b) antibody that binds and depletes mature mouse neutrophils and eosin-ophils (23). 2E6 is an IgG hamster MAb that inhibits extrav-asation by binding to the surface b-2 integrin molecules of mouse neutrophils, thereby blocking their interaction with the intercellular adhesion molecule 1 of the vascular endothelial cells (16). Seven- to 8-week-old female BALB/c (H-2d) mice were pur-chased from Simonsen Laboratories (Gilroy, Calif.). HeLa-229 cells were obtained from the American Type Culture Collec-tion (ATCC) (Rockville, Md.), and McCoy cells were from Viromed (Minneapolis, Minn.). These cells were grown as previously described (19). The hybridoma RB6-8C5 was a gif