Chlamydia abortus and Chlamydia pecorum are closely-related obligate intracellular bacteria that infect small ruminants. C. abortus is the causative agent of ovine enzootic abortion (OEA) which is the major cause of abortion in most sheep-rearing countries worldwide and zoonotic risk to humans whereas C. pecorum is often associated with subclinical enteric infections. There are reports of co-infection of sheep co-infected with C. abortus and C. pecorum. The nature of this co-infection in terms of protective host immunity is unknown.
Host immune control of C. abortus is strongly associated with IFN-γ production which can restrict bacterial growth via the induction of indoleamine 2,3-dioxygenase (IDO) which degrades intracellular pools of tryptophan (Trp), an essential amino acid. In contrast, little is known about host immune control of ruminant C. pecorum infection. The recent annotation of the C. abortus S26/3 and C. pecorum W73 genomes has revealed key differences in the ability of these bacteria to synthesise tryptophan: C. abortus lacks the Trp operon whilst C. pecorum has a Trp operon encoding the genes to synthesise Trp from anthranilate. We therefore hypothesised that C. pecorum will not exhibit high sensitivity to IFN-γ–mediated immune control.
To address this hypothesis we infected sheep and human cell lines with C. pecorum and C. abortus, exposed the cells to recombinant ovine and human IFN-γ respectively and monitored chlamydial growth by anti-LPS immunofluorescence and 16S RNA qCPR. Contrary to our hypothesis, IFN-γ did control the growth of C. pecorum in both sheep and human cell lines in a manner similar to C. abortus. Further experiments are underway to determine how this restriction of growth relates to intracellular IDO expression. These results indicate that immune control strategies targeting CD4+ve Th1 cells could be effective against C. abortus and C. pecorum.