Chlamydia pneumoniae Infects and Multiplies in Lymphocytes In Vitro

Abstract

The obligate intracellular pathogen Chlamydia (Chlamydophila) pneumoniae is known to be associated with some chronic inflammatory diseases, such as atherosclerosis. Interaction between C. pneumoniae and immune cells is important in the development of such diseases. However, susceptibility of immune cells, particularly lymphocytes, to C. pneumoniae infection has not been reported, even though lymphocytes play a pivotal role in the development of the diseases caused by this bacterium. In this regard, we examined the susceptibility of lymphocytes to C. pneumoniae infection in vitro. The results demonstrated that human peripheral blood lymphocytes as well as mouse spleen lymphocytes could be infected with C. pneumoniae. Furthermore, purified T lymphocytes as well as established T-lymphocyte cell line cells showed an obvious susceptibility to C. pneumoniae infection, indicating that T cells could be one of the host cells for this bacterial infection. These findings reveal a new infection site for C. pneumoniae, i.e., lymphocytes.Chlamydia (Chlamydophila) pneumoniae is an obligate intracellular bacterium which causes a variety of respiratory illnesses, including community-acquired pneumonia, bronchitis, pharyngitis, and sinusitis (25). Current studies also indicate the possible involvement of C. pneumoniae in chronic inflammatory as well as other diseases, such as asthma (10), arthritis (8), and atherosclerosis (23), besides respiratory illness. However, even though there are a large number of reports relating C. pneumoniae infection and certain chronic inflammatory diseases, the mechanisms for development of such diseases by Chlamydia infection is not clear. In the case of atherosclerosis, for instance, how Chlamydia organisms reach the intima, which is the main site of atherosclerosis, and how Chlamydia spp. are involved in the chronic inflammatory reaction characterized in atherosclerosis are not well understood. It is known that lymphocytes always play a central role in the development of chronic inflammatory diseases by their diverse functions. In this regard, a recent study by Kaul et al. (18) showed an interesting finding indicating that Chlamydia DNA could be recovered from CD3 ϩ peripheral blood leukocytes obtained from the patients attending a cardiology clinic. This finding suggests the possibility that lymphocytes may be a host cell for C. pneumoniae.Although C. pneumoniae is known to preferentially infect the epithelial tissue of the respiratory tract, this bacterium can also multiply in vitro in monocytes/macrophages, endothelial cells, and aortic smooth muscle cells (1,3,4,9,17,26). However, there are no reports regarding experimental in vitro infection of lymphocytes with C. pneumoniae which demonstrate that lymphocytes can be a host cell. The study reported here demonstrates that lymphocytes, particularly T lymphocytes, can be infected with C. pneumoniae and support the growth of this bacterium in vitro. These findings may reveal a possible new Chlamydia infection pathway, i.e., lymphocytes. MATERIAL...

Early cytokine profiles in the joint define pathogen clearance and severity of arthritis in Chlamydia‐induced arthritis in rats

“…It is a capture ELISA-based assay using a patented polymer chain-conjugated antibody technique and is as sensitive as current polymerase chain reaction (PCR) kits. This kit was originally developed for clinical use but has previously been used successfully in a murine experimental model (18).…”

“…Lewis and BN rats were killed 7 days postinjection, and the spleens were recovered and homogenized. The amount of Chlamydia was assayed using the Dako IDEIA PCE Chlamydia kit, adapted for use in rats (18).…”

Chlamydophila pneumoniae in human immortal Jurkat cells and primary lymphocytes uncontrolled by interferon-γ

“…Thus, it is When compared to Jurkat cells, C. pneumoniae did not grow well in human enriched peripheral blood lymphocytes. As supported by our previous studies showing successful inclusion formation and increased bacterial gene expression [16,18], it is obvious that C. pneumoniae could survive in human primary lymphocytes, but it is neglected just attaching and maintaining on the cell surface because of cell-free culture showing a rapid decrease of the bacterial infectious progenies below a detection limit. Alternatively, since it is well known that C. pneumoniae infection could induce TNF from monocytes/macrophages, which is a critical factor suppressing the bacterial growth in the cells [35,36].…”

“…trachomatis 434/Bu serovar L2 can infect and multiply in Jurkat human lymphocytes with a complete developmental cycle [16,17], and survive in human peripheral blood cells or mouse spleen cells [18][19][20], indicating that lymphocytes are a potential host cell for pathogenic chlamydiae. In the present study, we attempted to assess if lymphocytes could work as a shelter for C. pneumoniae to escape IFN-, which is a crucial factor for elimination of chlamydiae.…”

Chlamydophila pneumoniae attachment and infection in low proteoglycan expressing human lymphoid Jurkat cells

“…Maturation further occurs in the surrounding plasma membrane known as an inclusion [11][12][13]. Recently, our studies demonstrated that C. pneumoniae can infect and multiply in the human lymphocyte cell line Molt-4 and mouse spleen lymphocytes [14,15]. Furthermore, Kaul et al reported C. pneumoniae DNA in peripheral blood leukocytes obtained from cardiology patients [16].…”