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Leigh, P.C.J., Van Furth, R. and Zwet, T.L. (1986) In vitro determination of phagocytosis and intracellular killing by polymorphonuclear neutrophils and mononuclear phagocytes. In: Weir, D.M., Ed., Handbook of Experimental Immunology, 4th Edition, Blackwell Scientific Publications, 46, 1-46.

has been cited by the following article:

• TITLE: Studies of lead toxicity on inflammatory damage and innate immune functions in testicular macrophages of male Swiss albino mice

  AUTHORS: Shamim Ahmed S.K. Barbhuiya, Sumana Chakraborty, Mahuya Sengupta

  KEYWORDS: Lead; Phagocytosis; Intracellular Killing; Scanning Electron Microscopy; Proinflammatory Cytokines

  JOURNAL NAME: Modern Research in Inflammation, Vol.2 No.4, November 18, 2013

  ABSTRACT: Immune infertility has gained impetus in recent years. Various scientific studies have been carried out on the toxic effects of lead on immune function; however, uncertainties still persist. The present study addresses the immunomodulatory effects of testicular macrophages caused due to lead exposure (in-vivo). In mice, lead has a primary effect on the testes, and acts at all levels of the reproductive as well as the testicular immune response. The study was undertaken to investigate the effects of lead acetate on immune system in Swiss albino mice and the underlying mechanism of pro-inflammatory cytokine action. The immunomodulatory effects of lead are complex and appear to involve multiple pathways, not all of which are fully understood. Testicular macrophage dysfunctions by lead was studied by calculating morphological alteration and associated cell functions of innate immunity followed by estimation of pro-inflammatory cytokine release (TNF-α). The present work shows that lead is responsible for a significant morphological alteration, reducing cell function in testicular macrophages probably by increasing oxidative damage whereas increase in TNF-α release was also observed which increased inflammation. Results demonstrated that lead intoxication leads to increase in pro-inflammatory response. TNF-α is probably unable to bind with the surface receptor in testicular macrophages because of altered morphology which reduces cell function and ultimately causes reproductive dysfunction.