Heat shock proteins (HSP) were first identified in cells after exposure to elevated temperature. Subsequently HSP have been identified as a critical component of a very complex and highly conserved cellular defence mechanism to preserve cell survival under adverse environmental conditions. HSP are preferentially expressed in response to an array of insults, including hyperthermia, free oxygen radicals, heavy metals, ethanol, amino acid analogues, inflammation and infection. HSP interact with intracellular polypeptides and prevent their denaturation or incorrect assembly. In addition HSP are also involved in several processes essential for cellular function under physiological conditions. HSP production is enhanced during in-vitro embryo culture and they are among the first proteins produced during mammalian embryo growth. The spontaneous expression of HSP as an essential part of embryo development is well documented and the presence or absence of HSP influences various aspects of reproduction in many species. Finally, HSP are immunodominant antigens of numerous microbial pathogens, e.g. Chlamydia trachomatis, which have been recognized as the main cause of tubal infertility. Many couples with fertility problems have had a previous genital tract infection, have become sensitized to microbial HSP, and a prolonged and asymptomatic infection may trigger immunity to microbial HSP epitopes that are also expressed in man. Antibodies to both bacterial and human HSP are present at high titres in sera and hydrosalpinx fluid of many patients undergoing in-vitro fertilization (IVF). In a mouse in-vitro embryo culture model, these antibodies impaired the mouse embryo development at unique developmental stages. Recent studies indicate an association between a previous infection, immunity to HSP and reproductive failure.

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The role of Chlamydia (C.) trachomatis in male infertility is controversial. The objective of this study was to determine the prevalence of asymptomatic C. trachomatis infections in male partners of infertile couples, and to compare this result with the presence of chlamydial antibodies in serum and semen. C.trachomatis was detected in five of 50 semen specimens (10%) by either polymerase chain reaction for C. trachomatis DNA or direct DNA probing for C. trachomatis rRNA. There was no association between the detection of C. trachomatis in semen and the presence of chlamydial antibodies in serum or semen. Chlamydial serum antibodies were neither associated with antiserum serum antibodies nor with pathological standard semen parameters. These results indicate that the assessment of chlamydial immunoglobulin IgG and IgA antibodies in serum or semen is of limited use in male infertility work-up, in contrast to its significance in female tubal infertility. The presence of C. trachomatis in semen emphasizes the potential risk of transmission during artificial insemination and other assisted reproductive techniques, and underlines the importance of sensitive direct detection methods in this group of patients.

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