Impact of inflammation on male fertility

Front Biosci (Elite Ed). 2011 Jan 1;3:89-95. doi: 10.2741/e223.

Abstract

The male uro-genital tract is susceptible to gram-negative bacterial infections that produce a state of inflammation, particularly in the testis and epididymis. Development of germline stem cells into motile spermatozoa takes place in these organs and thus any impairment therein has a direct effect on male fertility. A number of factors are known to impair male fertility including environmental and chemical factors, lifestyle, and infections. The last is a little-known and poorly understood cause of male sub-/infertility. The presence of the pro-inflammatory cytokines like tumor necrosis factor-alpha (TNF- alpha), interleukin-1alpha (IL-1alpha) and interleukin-1beta (IL-1beta) in the male uro-genital tract following bacterial infections suggests that such infections could have cytokine-mediated anti-fertility effects. Furthermore, inflammation has been associated with elevated levels of reactive oxygen species and oxidative stress both of which affect male fertility. The present article summarizes the effects of inflammation on the testis, epididymis and spermatozoa. We review the correlations between inflammation and oxidative stress vis-à-vis spermatogenesis and discuss the implications of infections on male fertility/infertility and assisted reproductive technologies for the male.

MeSH terms

  • Epididymis / metabolism
  • Fertility / physiology*
  • Gram-Negative Bacterial Infections / complications
  • Gram-Negative Bacterial Infections / metabolism*
  • Humans
  • Inflammation / etiology
  • Inflammation / microbiology
  • Inflammation / physiopathology*
  • Interleukin-1alpha / metabolism
  • Interleukin-1beta / metabolism
  • Male
  • Male Urogenital Diseases / microbiology*
  • Oxidative Stress / physiology
  • Reactive Oxygen Species / metabolism
  • Spermatogenesis / physiology*
  • Spermatozoa / metabolism
  • Testis / metabolism
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Interleukin-1alpha
  • Interleukin-1beta
  • Reactive Oxygen Species
  • Tumor Necrosis Factor-alpha