Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0043167 (pertussis)
 19,595 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The different immunologic activities of lymph node and spleen cells as compared to peritoneal exudate cells were studied in temporarily desensitized, DNCB-contact-sensitive guinea pigs. Lymph node (and spleen) lymphocytes: (a) transfer contact sensitivity to syngeneic recipients when harvested at the time of unresponsiveness; (b) are only temporarily inactivated in tolerant recipients by the desensitizing procedure; (c) enter the lymph node (or spleen) compartments in a higher proportion than peritoneal exudate cells; (d) are not susceptible to inactivation in vitro; and (e) are not permanently desensitized when released into the circulation by an intravenous injection of Bordetella pertussis vaccine. These results indicate that the resistance of primed lymph node cells to the desensitizing procedure may account for the reappearance of contact sensitivity in desensitized guinea pigs.
J Invest Dermatol 1976 Jan
PMID:Mechanism of reappearance of contact sensitivity to DNCB in desensitized guinea pigs. 124 56

Atopic dermatitis (AD) is characterized by a variety of abnormal physiologic and pharmacologic responses in the skin. Leukocyte abnormalities of the cyclic nucleotide system include increased cAMP phosphodiesterase (PDE) and adenylyl cyclase activities. We have evaluated the possibility that a defect of the inhibitory GTP-binding protein (Gi) might cause inadequate modulation of adenylyl cyclase activity in AD leukocytes. We carried out a series of studies assessing adenylyl cyclase and Gi subunits in monocyte membranes. Using both pertussis toxin ribosylation and direct monoclonal antibody labeling of Gi proteins, we have shown evidence for a decrease or possible absence of one of the Gi proteins in atopic monocyte membranes. A genetic defect or toxin-mediated abnormality in leukocyte membrane Gi could account for these findings. Increased cAMP degradation by PDE may be a compensatory mechanism for increased cAMP synthesis that is regulated by GTP-binding proteins. But this increased PDE activity also rendered AD leukocytes hypo-responsive to immunofunction regulatory signals mediated by cAMP.
J Invest Dermatol 1992 Jun
PMID:Relationship between increased cyclic AMP-phosphodiesterase activity and abnormal adenylyl cyclase regulation in leukocytes from patients with atopic dermatitis. 131 24

Islet-activating protein (IAP), one of the pertussis toxins, serving [alpha-32P]nicotinamide adenine dinucleotide (NAD) as a substrate for ADP ribosylation, radiolabelled a specific pig epidermal membrane protein. The IAP-specific substrate was detectable by sodium dodecyl sulphate-polyacrylamide gel electrophoresis as a single band corresponding to a molecular weight of 40 kDa. The ADP ribosylation catalysed by IAP was inhibited by the addition of Mg2+ to the reaction mixture. IAP is known to work on intact cell systems resulting in the ADP ribosylation using intracellular NAD as the ADP ribose donor. Following IAP pretreatment of intact pig epidermis, the epidermal receptor adenylate cyclase responses were markedly increased; all the stimulatory receptor adenylate cyclase responses (beta-adrenergic, prostaglandin E, adenosine and histamine responses) were significantly increased. Cholera toxin-induced cyclic AMP accumulation was also significantly increased. Forskolin-induced cyclic AMP accumulation was slightly increased after IAP pretreatment, but this was not statistically significant. The IAP-dependent ADP ribosylation of the epidermal 40 kDa membrane protein, which was prepared from the IAP pretreated epidermis, was significantly decreased. It is known that the tumour promoter, phorbol 12-myristate,13-acetate (PMA), decreases stimulatory receptor adenylate cyclase responses of the epidermis. Following the PMA pretreatment, IAP-dependent ADP ribosylation of the epidermal membrane protein was unaffected. Furthermore, following the PMA pretreatment, the IAP-induced increase in the epidermal receptor adenylate cyclase responses still remained. Our results indicate that pig epidermis contains 40 kDa membrane substrate for IAP-dependent ADP ribosylation, which has an inhibitory tonus on the epidermal adenylate cyclase until its ADP ribosylation by IAP.(ABSTRACT TRUNCATED AT 250 WORDS)
Arch Dermatol Res 1990
PMID:Inhibitory guanine nucleotide binding protein in pig epidermis: regulation of epidermal adenylate cyclase. 196 35

The adenylate cyclase system of FRSK cells, a cultured cell line of fetal rat epidermal keratinocytes, and SV40-transformed human keratinocytes was investigated. Stimulators of the human epidermal adenylate cyclase, epinephrine, adenosine, and prostaglandin E2 increased cyclic AMP levels of these cells. There were marked differences in the stimulatory effects; while epinephrine revealed a much stronger effect than the other stimulators in FRSK cells, epinephrine and prostaglandin E2 revealed similarly marked effects in SV40-transformed cells. Histamine had little or only slight effect on the cyclic AMP levels of these cells. Cholera toxin and forskolin, which work on the stimulatory guanine nucleotide binding protein (Gs) and the catalytic component of adenylate cyclase, respectively, also increased cyclic AMP levels. Northern blot hybridization analysis revealed that both FRSK cells and SV40-transformed human keratinocytes express mRNAs for the beta 2-adrenergic receptor, as well as the stimulatory and inhibitory guanine nucleotide binding proteins (Gs and Gi, respectively). The presence of Gs as well as Gi were confirmed by cholera toxin-, and pertussis toxin (IAP)-induced ADP-ribosylation of membranous proteins of these cells. Our results indicate that both FRSK cells and SV40-transformed human keratinocytes express the fundamental components of the adenylate cyclase system. These cell lines might be useful tools for the analysis of the adenylate cyclase system in epidermal keratinocytes.
J Dermatol 1990 Aug
PMID:Adenylate cyclase system in fetal rat keratinizing epidermal cells (FRSK cells) and SV40-transformed human keratinocytes. 217 43

Keratinocyte expression of class II antigens (HLA-DR, human; Ia, murine) is associated with certain cutaneous diseases, especially those marked by the infiltration of immune and inflammatory cells into the skin. It has been shown that interferon-gamma (IFN-gamma) is capable of inducing human keratinocytes to express HLA-DR. Similar results, however, have not been duplicated in murine systems. The purpose of this study was to determine whether IFN-gamma was capable of inducing murine keratinocyte expression of Ia in vivo in an experimental model in which epithelial cells in a variety of organs were shown to express Ia after the i.v. injection of IFN-gamma. Recombinant murine IFN-gamma was injected into BALB/c mice. Biopsies of skin and intestine were analyzed by indirect immunoperoxidase to identify Ia-expressing keratinocytes and mucosal cells, respectively. Interferon-gamma was administered as either: 1) a single s.c. injection, 2) multiple i.v. injections of increasing doses (10(3)-10(5) U/d) on 3 consecutive d, or 3) i.p. injections of 5 X 10(4) U/d or 5 X 10(5) U/d on 6 consecutive d. At all i.v. and i.p. injection doses, the intestinal villi mucosal cells were induced to express Ia. Keratinocyte expression of Ia, however, was observed only in animals that received the two higher i.p. doses. Procedures to augment Ia expression, e.g., combined treatment with pertussis toxin, dinitrofluorobenzene, tumor necrosis factor, and indomethacin, did not enhance the ability of IFN-gamma to induce keratinocyte expression of Ia. We conclude that: 1) high doses of IFN-gamma are required to induce murine keratinocyte Ia expression in vivo and 2) low doses of IFN-gamma, although capable of inducing intestinal mucosal cells to express Ia, do not induce keratinocyte Ia expression.
J Invest Dermatol 1989 Jul
PMID:Differential expression of Ia by murine keratinocytes and gut epithelium in response to recombinant gamma-interferon. 230 58

The regulation of soluble phosphoinositide-specific phospholipase C from adult human epidermis by guanine nucleotide was investigated. In the presence of physiologic concentrations of Ca++ (1 microM) and Mg++ (1.5 mM), neither phosphatidylinositol (PI) nor phosphatidylinositol-4,5-bisphosphate (PIP2) were appreciably hydrolyzed. Addition of guanosine-5'-triphosphate (GTP) or guanosine-5'-O-(3-thiotriphosphate) (GTP-gamma-S) significantly stimulated hydrolysis of PIP2, but not PI. Stimulation of PIP2 hydrolysis by GTP was dose-dependent between 1-100 microM GTP. Other nucleoside triphosphates and nucleotide analogues were unable to substitute for GTP or GTP-gamma-S. A GTP-gamma-S-stimulated PIP2 hydrolysis was inhibited by guanosine-5'-O-(2-thiodiphosphate (GDP-beta-S). The phospholipase C preparation specifically bound [35S]GTP-gamma-S and this binding was also inhibited by GDP-beta-S. In addition to a 41,000-dalton pertussis toxin substrate, the phospholipase C preparation contained 3-4 GTP binding proteins with molecular weights between 20,000-30,000. These data demonstrate that human epidermis contains a soluble GTP-dependent phospholipase C activity that specifically hydrolyzes PIP2 and suggest that this reaction is regulated by a GTP-binding protein(s).
J Invest Dermatol 1989 Jun
PMID:GTP-dependent hydrolysis of phosphatidylinositol-4,5-bisphosphate by soluble phospholipase C from adult human epidermis. 254 16

Earlier experiments from our laboratory revealed that the medication most commonly used for depigmenting patients with vitiligo, monobenzyl ether of hydroquinone (MBEH), when applied to the skin of DBA/2 mice caused an increase in the population density (cells/mm2) of identifiable Ia+ and ATPase+ Langerhans cells. Further, this increase in Langerhans cell density could be correlated with an increase of contact hypersensitivity (CHS) reactivity to dinitrofluorobenzene (DNFB). The current experiments demonstrated that other compounds chemically similar to MBEH, such as butylated hydroxytoluene (BHT) and butylated hydroxyanisole (BHA), which are used as preservatives/antioxidants in many topical medications, cosmetics, food, and rubber products, can in five days significantly increase the population density of Thy-1+ dendritic epidermal cells. These compounds had no effects on Ia+ cells. This observation suggests that the Thy-1+ DEC cells may be more mobile and/or their surface markers may be readily expressed and are not a slowly mobile (trafficking) population of cells as suggested by the results of previous work. In addition, these parasubstituted phenolic compounds behaved like pertussis toxin and induced Thy-1 and Ia expression on keratinocytes. These changes in Thy-1 immune markers were not accompanied by functional alterations in the immune response to contact allergens as measured by the ear swelling technique.
J Invest Dermatol 1987 Nov
PMID:Rapid induction of Thy-1 antigenic markers on keratinocytes and epidermal immune cells in the skin of mice following topical treatment with common preservatives used in topical medications and in foods. 288 82

Three children had striking localization of varicella lesions to skin overlying a diphtheria-pertussis-tetanus toxoid (DPT) immunization injection site, a facial abrasion, and a sunburn of the trunk, respectively. Presumably, during the viremic stage of varicella, the virus passed from damaged blood vessels into the skin. A disabling myalgia in the thigh at the DPT site in one child may also have been the result of localization of the varicella virus in the muscle during the inapparent viremic stage. This suggests that an injection given during an occult viremia could trigger an unexpected reaction at the site.
Pediatr Dermatol 1987 Aug
PMID:Immunization, abrasion, and sunburn as localizing factors in chicken pox. 365 31

Eosinophils were shown to play a major role in the allergic inflammatory process leading to the clinical symptoms of atopic dermatitis. Only selected cytokines are capable of inducing a chemotactic response in eosinophils. In particular, the chemokine RANTES was recently shown to be a potent eosinophil chemotaxin. To examine the role of RANTES in eosinophil activation, we investigated the effect of RANTES and other chemokines on morphology and oxidative metabolism of highly purified eosinophils of normal nonatopic blood donors by assessment of functional as well as morphologic criteria. RANTES, and, to a lesser extent, MIP-1 alpha significantly induced the production of reactive oxygen species by human eosinophils, whereas MCP-1, MIP-1 beta, and interleukin (IL)-8/NAP-1 had no significant effects. RANTES stimulated only a subpopulation of the normal eosinophils. With the exception of IL-8, none of the cytokines tested had any significant effect on polymorphonuclear neutrophilic granulocytes. By scanning electron microscopy, RANTES induced characteristic changes that were completely abrogated in the presence of cytochalasin B. Based on functional and ultrastructural assays significant extracellular but not intracellular H2O2 production was detected and completely inhibited by cytochalasin B. Separation of eosinophils by discontinuous density gradients revealed the existence of two hypodense eosinophil populations, one which showed significantly reduced responses upon stimulation with RANTES. RANTES-induced production of reactive oxygen species was almost completely inhibited by staurosporine, wortmannin, or pertussis toxin. Based on these data it is evident that RANTES represents a potent eosinophil-specific activator of oxidative metabolism. Besides its chemotactic activity on T cells and eosinophils, therefore, RANTES may be involved in the functional activation of eosinophils in the skin of patients with atopic dermatitis.
J Invest Dermatol 1994 Jun
PMID:The chemokine RANTES is more than a chemoattractant: characterization of its effect on human eosinophil oxidative metabolism and morphology in comparison with IL-5 and GM-CSF. 751 98

The effects of staphylococcal enterotoxin B (SEB), a Staphylococcus aureus-derived bacterial superantigen, on expression of intercellular adhesion molecule-1 (ICAM-1) were examined in cultured normal and transformed (DJM-1 cells) human keratinocytes by flow cytometry, confocal microscopy, digital image processing, and reverse transcriptase-polymerase chain reaction. SEB significantly upregulated ICAM-1 expression in the interferon-gamma (IFN-gamma)-pretreated, HLA-DR-positive normal keratinocytes and DJM-1 cells in a dose-dependent manner, but not in the untreated, HLA-DR-negative cells. Other toxins such as diphtheria and pertussis toxins did not have the effect. The distribution of SEB and HLA-DR molecules was identical on the IFN-gamma-treated, HLA-DR-positive DJM-1 cells by confocal microscopy. Digital image processing analysis demonstrated that SEB induced a transient increase of intracellular calcium concentration only in the IFN-gamma-treated DJM-1 cells. Pretreatment of the IFN-gamma-treated DJM-1 cells with anti-major histocompatibility complex class II monoclonal antibody completely blocked the effect of SEB. Furthermore, ICAM-1 mRNA was detected in the IFN-gamma-pretreated, SEB-exposed normal keratinocytes by reverse transcriptase-polymerase chain reaction. Our results demonstrate that SEB binds to keratinocytes, presumably via major histocompatibility complex class II molecules such as HLA-DR, triggers calcium mobilization, and induces the synthesis of ICAM-1 molecules. We speculate that, in various cutaneous disorders, SEB penetrates the epidermis and interacts with HLA-DR-positive keratinocytes to upregulate ICAM-1 expression, thus modulating the course of the inflammatory process.
J Invest Dermatol 1995 Oct
PMID:Staphylococcal enterotoxin B upregulates expression of ICAM-1 molecules on IFN-gamma-treated keratinocytes and keratinocyte cell lines. 756 Nov 55


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