Immune effects

Immunotoxicity. Limited information is available regarding the effects of endosulfan on the human immune system. However, specially designed studies using rats indicate that both humoral and cellular immune responses are depressed by ingested endosulfan at doses that do not induce any overt signs of toxicity (Banerjee and Hussain 1986,1987). In vitro studies support the possibility that endosulfan affects immune system function (Das et al. 1988). These results demonstrate that immunotoxicity may be a more sensitive end point of endosulfan-induced toxicity than other end points, and humans may be at risk for adverse immune effects following exposure to endosulfan. An intermediate-duration oral MRL was derived based on the observation of depressed immune responses (Banerjee and Hussain 1987). 

Vos JG, Krajnc El, Beekhof PK, et al. 1982. Methods for testing immune effects of toxic chemicals Evaluation of the immunotoxicity of various pesticides in the rat. In Miyamoto J, Kearney PC, eds. Pesticide chemistry Human welfare and the environment. Oxford, England Pergamon Press, 497-504. 

Lebrec, H. et al., Immunotoxicological investigation using pharmaceutical drugs. In vitro evaluation of immune effects using rodent or human immune cells, Toxicology, 96, 147, 1995. 

Krieg, A.M., CpG motifs in bacterial DNA and their immune effects, Annu. Rev Immunol, 20, 709, 2002. 

There is considerable interest in the role of infectious agents in the development of autoimmune diseases. Some of this interest is based on the concept of molecular mimicry as a causal mechanism. Molecular mimicry refers to the possible pathologic role of cross-reactive antibodies or T cells to a self-antigen that is structurally similar to, and thus shares epitopes with, a viral or other infectious agent. For most autoimmune diseases, however, evidence of molecular mimicry leading to disease is not conclusive.1819 Viruses and other infections also have a less-specific immune effect, stimulating toll-like receptors and proinflammatory cytokine secretion, which is another mechanism that has been postulated to influence autoimmune disease risk.20... 

Ezendam, J., Vos, J., and Pieters, R., Mechanisms of Hexachlorobenzene-induced adverse immune effects in Brown Norway rats. J. Immunotoxicol., 1, 167, 2004. 

Ezendam, J. et al., Macrophages are involved in hexachlorobenzene-induced adverse immune effects. Toxicol. Appl. Pharmacol., 209, 19, 2005. 

It has been suggested that lactoferrin may only confer beneficial immune effects when consumed in the form of breast milk (Lonnerdal, 2003). When added to infant formula, lactoferrin may be affected by its prior bioactivity how it was added (blended or dissolved) and extent of heat treatment of the formula (Lonnerdal, 2003). There is evidence that lactoferrin can be inactivated by invading pathogens or even enhance microbial pathogenicity. For example, the pneumococcal surface protein A of Streptococcus pneumoniae was reported to bind to lactoferrin and protect the bacteria from the killing action of lactoferrin (Ward et ah, 2005). 

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