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Endogenous IFN- Production Is Induced and Required for Protective Immunity against Pulmonary Chlamydial Infection in Neonatal Mice¹

Madhulika Jupelli^*, M. Neal Guentzel^*, Patricia A. Meier, Guangming Zhong, Ashlesh K. Murthy^* and Bernard P. Arulanandam^2,*

^* South Texas Center for Emerging Infectious Diseases, Department of Biology, University of Texas, San Antonio, TX 78249; Department of Pathology, Wilford Hall Medical Center, San Antonio, TX 78236; and Department of Microbiology and Immunology, University of Texas Health Science Center, San Antonio, TX 78229

Chlamydia trachomatis infection in neonates, not adults, has been associated with the development of chronic respiratory sequelae. Adult chlamydial infections induce Th1-type responses that subsequently clear the infection, whereas the neonatal immune milieu in general has been reported to be biased toward Th2-type responses. We examined the protective immune responses against intranasal Chlamydia muridarum challenge in 1-day-old C57BL/6 and BALB/c mice. Infected C57BL/6 pups displayed earlier chlamydial clearance (day 14) compared with BALB/c pups (day 21). However, challenged C57BL/6 pups exhibited prolonged deficits in body weight gain (days 12–30) compared with BALB/c pups (days 9–12), which correlated with continual pulmonary cellular infiltration. Both strains exhibited a robust Th1-type response, including elevated titers of serum antichlamydial IgG2a and IgG2b, not IgG1, and elevated levels of splenic C. muridarum-specific IFN-, not IL-4, production. Additionally, elevated IFN-, not IL-4 expression, was observed locally in the infected lungs of both mouse strains. The immune responses in C57BL/6 pups were significantly greater compared with BALB/c pups after chlamydial challenge. Importantly, infected mice deficient in IFN- or IFN- receptor demonstrated enhanced chlamydial dissemination, and 100% of animals died by 2 wk postchallenge. Collectively, these results indicate that neonatal pulmonary chlamydial infection induces a robust Th1-type response, with elevated pulmonary IFN- production, and that endogenous IFN- is important in protection against this infection. The enhanced IFN- induction in the immature neonatal lung also may be relevant to the development of respiratory sequelae in adult life.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by National Institutes of Health Grant SO6GM008194-24.

² Address correspondence and reprint requests to Dr. Bernard Arulanandam, Department of Biology, South Texas Center for Emerging Infectious Diseases, University of Texas, One University of Texas San Antonio Circle, San Antonio, TX 78249. E-mail address: Bernard.arulanandam{at}utsa.edu

³ Abbreviations used in this paper: i.n., intranasal; HEL, hen egg lysozyme; IFU, inclusion forming unit.

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