S1C12P2Neutrophils


S1C12P2-1: Infiltrates of neutrophils (i.e., acute inflammation) are encountered in a wide variety of settings. The neutrophil is the prime reacting cell in many infections, particularly the bacterial infections. It is the prime reacting cell in responses to acute injury. It is the chief reacting cell along the complement cascade in response to antigen-antibody complexes. As in this field, neutrophils may collect in defects without a significant breakdown of cells, or release of digestive enzymes. Neutrophils have collected in a subcorneal defect; the character of the keratin layer has been little affected. The widened inter-cellular spaces in the epidermis are evidence of inter-cellular edema. The cells among the keratinocytes are lymphocytes and histiocytes.

S1C12P2-2: If neutrophils are activated, they die and disintegrate; in the acts, damaging catalytic enzymes will be released into the tissue. In this peri-follicular region, infiltrates of neutrophils and histiocytes extend through a follicular defect into the neighboring reticular dermis. Collagen bundles of the dermis have been digested; inflammatory cells and cellular debris have collected in the defect; the pattern is one of a lytic, neutrophilic collagenosis. The basophilic debris is a product of the lytic process; the basophilia is contributed by the breakdown of the nuclei of neutrophils. Nucleic acids impregnate the necrotic debris. Light blue arrows identify elastic fibers; the elastic fibers are more resistant to the effects of the digestive enzymes than are the collagen bundles. This is a common pattern in the category of acneiform folliculitides (acneiform folliculitis with perforation).

S1C12P2-3: In the area of the green arrows, hyperplastic follicular epithelium abuts upon the reticular dermis without a supporting stroma (peri-follicular connective tissue sheath). This relationship qualifies the pattern as a variation of pseudoepitheliomatous hyperplasia. A defect extends from the lumen of the follicle on the left through the epithelial lining of the follicle into the reticular dermis on the right. The defect contains neutrophils. On the right, at the interface with the reticular dermis, the neutrophils of the infiltrates have disintegrated. The resulting debris is deeply basophilic (heavily impregnated with nucleic acids of the destroyed nuclei of neutrophils) (acneiform folliculitis with perforation).

S1C12P2-4: In this field, a defect extends from right to left; it extends from the region of a follicle into the reticular dermis. It is lined by an extension of hyperplastic squamous epithelium of follicular origin. The defect contains neutrophils and basophilic debris. In the region of the green arrows, an elastic fiber “perforates” the epithelium. Actually the epithelium perforates the dermis without inducing a stroma; in its progress from right to left, it has entrapped connective tissue fibers. The connective tissue is passive; the epithelium is the mobile component. The invasion of the dermis in this manner by benign epithelium (i.e., epithelium which sits on retinacular tissue rather than stroma (adventitial dermis) is a basic feature of the form of invasive epithelial hyperplasia that is characterized as pseudoepitheliomatous (in this example, a perforating folliculitis is represented).

S1C12P2-5: This is a variation of the patterns of acute inflammation. In this example, the neutrophil is the preponderant reacting cell; neutrophils have collected in the papillary dermis. By the process of death and degeneration of neutrophils, the inflammation has altered the relationships between epithelium and stroma (papillary dermis). The epidermis has separated from the dermis to produce a sub-epidermal vesicle; the vesicle contains a loose infiltrate of neutrophils ( dermatitis herpetiformis: DH). The damage involves the basement membrane zone as well as basal keratinocytes. To the left, the defect is multi-loculated.

S1C12P2-6: At the margin of any vesicle, there generally will be more clues regarding the pathogenesis of the lesion than will be available from an examination of the floor of the vesicle centrally. In this field, separations have occurred at the tips of dermal papillae. Neutrophils and eosinophils (red arrows) are clustered along the floor of the defects and in the dermal infiltrates. The dermal papillae show a smudgy alteration of connective tissue (above green arrows) and there is poor (pale) staining of the nuclei of migratory histiocytes. There are fragments of nuclear debris. The breakdown of inflammatory cells has released digestive enzymes; the enzymes have partially digested the connective tissue of the dermal papillae and of the basement membrane zone. As a result, the cohesive components have released their grip on the epidermis. The epidermis has separated from the dermis ( DH).

S1C12P2-7: This is an earlier pattern of DH. The papillae and supra-papillary defects are more uniformly cellular. This example is rich in eosinophils. Blue arrows identify a zone of early supra-papillary clefting . To the left of the center of the field, infiltrates of eosinophils, neutrophils and other inflammatory cells have collected in irregular defects in the basal unit of the epidermis; the inflammation has produced cytolytic changes affecting keratinocytes in the hyperplastic basal unit of the epidermis.

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