PubMed · 1049933
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R J Rycroft. 1976-10-21. Dermatitis.. https://pubmed.ncbi.nlm.nih.gov/1049933/
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Acute inflammatory reactions are characterized by leukocyte infiltration associated with increases in vascular permeability and in local blood flow. Leukocyte infiltration can be induced by chemotactic factors such as leukotriene B4 (LTB4) and paf-acether (formerly known as platelet-activating factor) that can be generated within inflammatory lesions. Vascular permeability and increase in blood flow are also affected by LTB4 and paf-acether, as well as by several other substances, including histamine and prostaglandins. Derived from arachidonic acid via the 5 lipo-oxygenase pathway, LTB4 is one of the most potent leukocyte chemotactic substances known. Intradermal injections of LTB4 induce dermal neutrophil infiltration in animal models and in humans. Topical application of LTB4 to human skin induces intraepidermal micro-abscesses containing numerous intact neutrophils. LTB4 has been found to be increased in psoriatic lesions, but its synthesis by epidermal cells remains undecided. Like other leukotrienes, LTB4 can stimulate DNA synthesis in cultured human epidermal keratinocytes. However, receptors for LTC4 but not for LTB4 have been found on human keratinocytes in culture. Paf-acether is an ether-linked phospholipid identified as 1-O-alkyl-2-O-acetyl-sn-glycero-3-phosphocholine and is considered to be one of the most potent mediators of acute allergic and inflammatory reactions. For instance, intradermal injection of paf-acether induces inflammatory events such as neutrophil infiltration and increase in vascular permeability. Recent data suggest that cutaneous cells, such as fibroblasts and keratinocytes, are capable of producing paf and that paf is released during the development of allergic cutaneous reactions.(ABSTRACT TRUNCATED AT 250 WORDS)
BACKGROUND: Lichen nitidus is believed, by some, to be a variant of lichen planus, and by others to be a distinct entity. OBJECTIVE: We examined five cases of lichen nitidus with immunohistochemical reagents designed to characterize the dermal inflammatory infiltrate in an attempt to resolve the uncertainty. METHODS: We stained formalin-fixed, paraffin-embedded tissue sections with the following antibodies: L26, A6, KP1, BerH2, OPD4, and HECA-452. RESULTS: The inflammatory infiltrate was 90% A6+, with few L26+ cells. In contrast to lichen planus, KP1+ macrophages were seen and fewer of the lymphocytes demonstrated HECA-452. Fifty percent to 80% of lymphocytes were OPD4 positive, similar to that usually seen in lichen planus. Rare Ki-1+ cells were seen in one case. CONCLUSION: We believe that the pattern of a mixed cellular infiltrate characterized by macrophages and a helper T cell response with few HECA-452+ cells is somewhat different from the pattern seen in lichen planus, wherein almost all of the cells are CD4+/HECA-452+ lymphocytes. This suggests a different immunologic pathogenesis.
Superoxide and hydrogen peroxide are reactive oxygen species (ROS) primarily produced by phagocytic cells as a consequence of the process of phagocytosis. This defensive role, may, however, become one of attack when production of ROS is excessive and overwhelms cellular scavenging systems. This happens in situations such as acute inflammation and results in host cell membrane damage, which is particularly prevalent in the presence of transition metal catalysts such as iron and copper. The skin is uniquely vulnerable to this attack being rich in polyunsaturated fatty acids and exposed to high oxygen tensions and ultraviolet light, both of which promote production of ROS. Additionally, the respiratory burst of infiltrating polymorphonuclear leukocytes and macrophages in inflamed skin will produce high local levels of superoxide that can release "catalytic iron" from storage proteins such as ferritin. The role of iron and ROS in the pathogenesis of inflammatory skin disease is discussed as is the possibility of novel therapeutic strategies based on their removal.