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Biomedical subjects

K J Bloch

Publications and source records attributed to K J Bloch.

At least 19 recordsLinked to original sources
PubMed1992

Reduction in biliary IgA after burn injury. Role of diminished delivery via the thoracic duct and of enhanced loss from the systemic circulation.

The concentration of biliary IgA is greatly reduced after scald burn injury in the rat, thereby contributing to a deficiency in upper intestinal immune defense. This reduction in biliary IgA might have several explanations, including failure of the transhepatic transport of polymeric IgA (pIgA) from the circulation, decreased delivery of pIgA to the hepatocyte, or decreased local synthesis of IgA in the liver. The authors examined whether burn injury reduces circulating pIgA available for delivery to the hepatocyte. In initial studies, they demonstrated that burn injury induces a decrease in circulating pIgA in bile-duct-ligated rats. They then sought to determine whether this decrease in pIgA was due to increased loss from the circulation or to a decreased supply of pIgA to the circulation through the thoracic duct. After injection of purified 125I-pIgA into bile duct-ligated rats, radioactivity was removed more rapidly from the circulation of burn-injured compared with control rats. The radioactivity localized in the skin and muscle at the site of burn injury. In another group of rats with patent bile ducts, the thoracic duct was cannulated and lymph collected for 12 hours. The total amount of IgA protein in lymph was found to be reduced in burn-injured compared with control animals. Thus, burn injury is accompanied by reduced circulating pIgA, which may be attributed to its enhanced loss from the circulation and to decreased delivery of pIgA from the intestinal mucosa to the systemic circulation via the thoracic duct.

Animals↗
PubMed1992

Effect of thermal injury on transfer of IR22 IgA myeloma protein into bile in the rat.

We previously observed a 75-90% decrease in concentration of biliary IgA after thermal injury to rat skin. Decrease in biliary IgA might result from an alteration in supply of polymeric IgA delivered to the hepatocyte or from an alteration in hepatocyte transfer of polymeric IgA into bile. In the present study, we examined the transfer of intravenously administered 125I-IgA into bile. Purified IR22 rat IgA myeloma protein consisting of both monomeric and polymeric IgA was labelled with 125I. Sprague-Dawley rats (140-180 g) received a 20-30% body surface area scald-burn or sham treatment. The bile duct was cannulated 18-24 h later and 125I-IgA preparations were injected into the tail vein. Bile was collected under light ether anesthesia for 3 h. In rats injected with 125I-IR22 IgA myeloma protein there were no significant differences in total, TCA-precipitable, or immunoprecipitable radioactivity in bile from burn-injured or sham-treated animals. On Bio-Gel A-1.5 m gel permeation, the radioactivity in bile from sham-treated animals eluted in the region of polymeric IgA as expected; the radioactivity in the bile from burn-injured animals eluted equally in the same regions as polymeric IgA and monomeric IgA. In sham-treated rats injected with isolated polymeric IgA only, bile contained primarily polymeric IgA. In burn-injured rats injected with polymeric IgA only, bile contained a mixture of polymeric IgA and monomeric IgA. These findings suggest that hepatocyte processing of polymeric IgA is altered after thermal injury, resulting in the transformation of some polymeric IgA into its monomeric form.

Animals↗
PubMed1992

Vascular permeability during the early and late phases of ocular anaphylaxis.

The role of enhanced vascular permeability in a model of ocular anaphylaxis was investigated during both early- and late-phase reactions (EPR and LPR). Vascular permeability was assessed by measuring the extravascular retention of 125I-bovine serum albumin (125I-BSA) in ocular tissues. Ten groups of guinea pigs (n = 5-12 per group) were injected with dinitrophenylated (DNP) bovine gamma globulin emulsified in Freund's adjuvants and challenged after a 4-week interval by topical application of di-DNP-lysine to one eye and phosphate-buffered saline to the other eye. Thereafter, the eyes were examined and the animals were killed at different intervals after topical challenge. They were injected intravenously with 125I-BSA 0.5 hr before death. Retained radioactivity was measured separately in four tissues. The EPR (period between 0.5-1.5 hr after challenge) was characterized by enhanced retention of radioactivity in lids, conjunctiva, and orbital content. There was no significant retention of extravascular radioactivity in the globe and lacrimal gland. Thereafter (period between 2-3.5 hr after challenge), retained radioactivity was significantly diminished. The subsequent period, between 4.5-6.5 hr (LPR), was characterized by a smaller, although significant, increment of radioactivity retained in lids and conjunctiva but not in the other tissues examined. These findings indicate that enhanced microvascular permeability occurs during two phases in actively immunized guinea pigs challenged topically with di-DNP-lysine and that these phases correspond to the clinical signs that constitute the EPR and LPR of ocular anaphylaxis.

Anaphylaxis↗
PubMed1991

Inhibition of immune complex-induced enteropathy by three different platelet-activating factor receptor antagonists.

We previously showed that intravenous injection of rat anti-BSA-BSA complexes (IC) prepared in 5x antigen excess rapidly induced a striate pattern of serosal (to mucosal) hemorrhage and vascular congestion throughout the small intestine of the Sprague-Dawley rat. In this study, we tested the effect of three different platelet-activating factor (PAF) receptor antagonists on the development of lesions. L-652,731, a synthetic derivative of kadsurenone (at doses of 1.3-2.7 mg/kg), SRI 63-675, a substituted quinolinium compound (6.7-15 mg/kg), and WEB 2086, a thienotriazolodiazepine (5-25 mg/kg) were each capable of completely or partially inhibiting IC-induced enteropathy in the majority of animals tested. Pretreatment with WEB 2086 prevented IC-induced hemoconcentration but not neutropenia. The antagonists did not lower the level of blood complement nor interfere with the fall in complement induced by administration of IC. The ability of PAF receptor antagonists to completely or partially inhibit IC-induced small intestinal lesions suggests that endogenous PAF is a major mediator of IC-induced enteropathy.

Animals↗
PubMed1991

Schnitzler's syndrome: a broader clinical spectrum.

Schnitzler's syndrome is characterized by chronic urticaria, recurrent fever, bone pain, and lymphadenopathy in conjunction with a serum IgM M component in a concentration that is usually less than 10,000 mg/L. Complement activation and cryoprecipitation do not appear to be involved. We report two additional patients who share many of the characteristics of this entity. These patients differ from patients previously reported because of the markedly elevated IgM M-component concentration in one patient and the severity of anemia in the second patient. An increased frequency of IgG autoantibodies to interleukin-1-alpha has been reported by other investigators; it has been suggested that an antibody-mediated prolongation of the half-life of interleukin-1-alpha might account for some of the symptoms and signs of this disorder. However, neither the mediators involved in the induction of nonpruritic urticaria nor the role of the IgM M component has been established.

Back Pain↗
PubMed1991

Leukotrienes, thromboxane A2, and prostaglandins during systemic anaphylaxis in sheep.

We investigated the roles of eicosanoid mediators in acute systemic anaphylaxis in anesthetized sheep. Sheep were sensitized with dinitrophenylated Ascaris suum extract and were challenged with an intravenous injection of dinitrophenylated bovine serum albumin. During anaphylaxis, cyclooxygenase inhibitors eliminated the elevation of arterial plasma levels of thromboxane B2 and 6-ketoprostaglandin F 1 alpha but markedly elevated the levels of leukotriene E4 in lung lymph without significantly eliminating elevation of plasma levels of histamine. Most of the measured physiological abnormalities accompanying anaphylaxis were aggravated by cyclooxygenase blockade. Enhancement of this anaphylactic mediator response was associated with an accentuated and prolonged increase of airway pressure (P less than 0.05, compared with sensitized, antigen-challenged but otherwise untreated sheep), a more intense hypoxemia (P less than 0.0001), and leukopenia (P less than 0.001), changes that were largely eliminated by pretreating with the sulfidopeptide leukotriene (SPLT) antagonist FPL 55712, suggesting that the SPLTs were important mediators of these responses. In contrast, the prolonged, but less severe, systemic vascular collapse and the reduced pulmonary hypertension induced by cyclooxygenase inhibitors were not influenced by the SPLT antagonist. These results demonstrate that in sheep cyclooxygenase metabolites are mainly involved in the acute, but transient, systemic and pulmonary vascular response of systemic anaphylaxis, whereas SPLTs are primarily implicated in the airway and secondary cardiovascular response. SPLT may act either directly or by potentiating the release of and reactivity to histamine and other mediators. Our data therefore suggest that a combination of cyclooxygenase and lipoxygenase inhibition will be necessary to more effectively protect against the consequences of an anaphylactic reaction.

6-Ketoprostaglandin F1 alpha↗
PubMed1991

Expression of MHC class II (Ia) antigen by the neonatal enterocyte: the effect of treatment with interferon-gamma.

Immunohistochemical techniques were used to probe the expression and inducibility of class II major histocompatibility complex (MHC) (Ia) antigens by the mouse enterocyte at various stages postpartum. Expression of Ia was related to both age and intestinal location. Ia antigen was not detected until at least 1 week post-weaning and was noted thereafter in both proximal and distal intestine. Both crypt and villus enterocytes were stained in the distal small intestine, but staining was restricted to the upper portion of the villus in the proximal small intestine. Moreover, the extent of staining and the intensity of staining were greater in the distal small intestine. The effect of a single injection of recombinant mouse interferon-gamma (IFN-gamma) on Ia expression by enterocytes of 16-day-old, suckling BDF1 mice was examined. Injection of distilled water (DW) or 1 to 2 x 10(4) U IFN-gamma did not induce enterocyte Ia expression. Doses of 4-10 x 10(4) U were effective inducers of Ia on crypt and, occasionally, on lower villus cells examined 24 hr later. Staining did not persist on the enterocyte beyond 48 hr. In conclusion, Ia is not normally expressed on small intestinal enterocytes of the mouse until after weaning; however, Ia expression can be induced earlier by treatment with IFN-gamma. It is not known whether failure to detect Ia expression prior to weaning reflects a lack of positive stimuli and/or the presence of inhibitory stimuli, possibly carried in the breast milk.

Aging↗
PubMed1990

Divalent hapten-induced intestinal anaphylaxis in the mouse enhances macromolecular uptake from the stomach.

The capacity of the stomach to participate in anaphylaxis induced by the hapten N,N'-di-2,4,dinitrophenyllysine (di-DNP-lysine) was examined in BDF1 female mice immunized with dinitrophenylated Ascaris suum extract. Immunized animals underwent laparotomy and nontraumatic pyloric occlusion using a microvascular clamp. Following wound closure, animals were gavage-fed ovalbumin together with di-DNP-lysine. Other mice were subjected to systemic anaphylaxis by intravenous injection of di-DNP-lysine administered 1 min after gavage feeding of ovalbumin. The intravenous and intragastric administration of di-DNP-lysine led to a sixfold or greater increase in serum immunoreactive ovalbumin. Examination of 1-micron sections of gastric tissue from DNP-Asc-immunized and unimmunized mice showed an intact mucosal and submucosal architecture. A 75% increase in the number of mast cells below the muscularis mucosa was seen in immunized compared with unimmunized BDF1 mice. Gastric tissue sections from immunized mice challenged orally or intravenously with di-DNP-lysine showed compaction of erythrocytes in blood vessels, degranulation of mast cells, degenerative changes in the gastric epithelium, expulsion of mucus from gastric glands, and edema in the lamina propria. The present model may be useful for further defining the consequences of anaphylaxis on the development of immune responses to dietary antigens.

Anaphylaxis↗
PubMed1990

Anaphylaxis during induction of general anesthesia: subsequent evaluation and management.

Twenty-seven patients were referred for evaluation of anaphylaxis after induction of general anesthesia (GA) in which thiobarbiturates, muscle relaxants, or antibiotics were administered intravenously. Skin testing by the prick and intracutaneous methods was performed with dilutions of the thiobarbiturates and muscle relaxants; beta-lactam reagents were used in patients who had also received these drugs. No skin test reactivity was noted in 16 normal subjects. Skin tests were positive in 13 patients (thiobarbiturates in five, muscle relaxants in six, and antibiotics in two patients). Two patients were dermatographic and yielded indeterminate skin test results. Eleven of the 27 patients subsequently had GA; all patients received a premedication regimen of prednisone and diphenhydramine. Of three patients with negative skin tests, one experienced an arrhythmia, but no other signs attributable to anaphylaxis were noted. One patient with dermatographism had GA without a reaction. Positive skin tests implicated an agent that was avoided in seven patients; one of these patients experienced delayed urticaria/angioedema after the completion of GA. Thus, no patients developed anaphylaxis during subsequent GA for which agents producing positive skin tests were avoided, and a premedication regimen was used.

Adolescent↗
PubMed1990

Early and late phases of ocular anaphylaxis in actively immunized guinea pigs.

A model of ocular anaphylaxis with distinct early- and late-phase components was studied in actively immunized guinea pigs. Twenty guinea pigs were injected with dinitrophenylated (DNP) bovine gamma globulin emulsified in Freund's complete adjuvant and challenged topically with di-DNP-lysine. Clinical signs were monitored over a 48 h period. An early-phase reaction (EPR) characterized by conjunctival edema, conjunctival erythema, lid swelling, and lid redness was observed. This reaction peaked at 0.5 h after challenge and subsided to a low point at 3-4 h. Subsequently, a second episode of lid swelling and lid redness was observed at 4-8 h. All animals in both groups exhibited an EPR. In addition, 75% of the animals underwent an EPR and an LPR. No animals exhibited an isolated LPR. Of the animals that underwent a dual response, 47% were biphasic, 6% were prolonged and 47% were multiphasic. The development of an active model of ocular anaphylaxis exhibiting both EPR and LPR components will enable studies of mechanisms which regulate the frequency and magnitude of these ocular allergic responses.

Anaphylaxis↗
PubMed1990

Clinical patterns of ocular anaphylaxis in guinea pigs passively sensitized with IgG1 antibody.

A model of topically induced ocular anaphylaxis in guinea pigs was developed. A guinea pig anti-dinitrophenyl (DNP) bovine gamma-globulin antiserum rich in IgG1 antibodies was injected subconjunctivally; various serum dilutions and latent periods were tested. The anaphylactic response was elicited with di-DNP-lysine applied topically. The response was characterized by rating 11 ocular signs. Although the 4-hour latent period is considered optimal for passive cutaneous anaphylaxis, a 14-hour latent period yielded the strongest ocular reaction and appeared to the most appropriate time for clinical assessment. Both an early-phase reaction (peaking in the 21st hour) and a late-phase reaction (peaking at 6-10 h) were observed. The two signs of the early-phase reaction that recurred in the late-phase reaction were periorbital swelling and lid redness. The anaphylactic reaction displayed different patterns in different animals: protracted, biphasic and multiphasic.

Anaphylaxis↗
PubMed1990

Determination of the interval during which one application of compound 48/80 to the rat conjunctiva influences the response to a second application.

We studied the effect of one application of compound 48/80 to the conjunctiva of the rat on the response to a subsequent challenge. Rats treated once showed conjunctival edema and marked degranulation of conjunctival mast cells. A second exposure to compound 48/80, applied after an interval of 24 h, produced slight clinical effects but had marked effects on conjunctival mast cells. Approximately 90% of the mast cells could no longer be observed by light microscopy. As the interval between initial challenge and rechallenge was increased, the clinical response returned, mast cells were again observable in normal numbers, and the extent of degranulation returned to approximately 50%. After an interval of 7 days, rats responded clinically as they had to the first application of compound 48/80. Although the number of mast cells in the conjunctiva was normal and extensive degranulation occurred, exocytosis was not observed. Thus some effects of the first application of compound 48/80 persisted for at least 1 week. Whether the effects observed depend upon the continued presence of compound 48/80 in the mast cell or granule membrane remains to be determined.

Analysis of Variance↗
PubMed1990

Histology of ocular late-phase reaction in guinea pigs passively sensitized with IgG1 antibodies.

The ocular late-phase reaction (LPR) is a mast cell-dependent, delayed inflammatory reaction developing 4-12 h after the early-phase reaction (EPR). We developed a passive IgG1 antibody-dependent guinea pig model that clinically reproduced the biphasic reaction of ocular EPR and LPR. An EPR was observed in all animals; a biphasic, multiphasic or prolonged inflammation was observed in the animals maintained for 9 and 24 h. The substantia propria of eyes undergoing EPR (0.5 h) showed intense edema, mast cell degranulation (88%), and 4-fold increase in eosinophils. At 9 h, the neutrophils and eosinophils had increased 11- and 25-fold, respectively. The number of basophils and lymphocytes was significantly increased compared to the controls (p less than 0.05). Of the mast cells, 45% were degranulated compared with 19% for controls. Cellular reactions had subsided by 24 h. Conjunctival epithelium also accumulated inflammatory cells as did the stroma of the lid skin. These histologic changes in ocular tissues undergoing anaphylaxis demonstrated that mast cell degranulation was most severe in the early phase, whereas neutrophil, eosinophil, and basophil accumulation was most marked in the late phase.

Animals↗
PubMed1990

Effect of topical dexamethasone on the ocular allergic reaction in passively sensitized guinea pigs.

We examined the effect of extended topical pretreatment with dexamethasone (Dex) on the ocular allergic response in passively sensitized guinea pigs. The passive IgG1 antibody dependent guinea pig model used in these studies demonstrates both early- and late-phase ocular anaphylactic reactions. Fourteen hours prior to challenge with the hapten di-DNP-lysine, three groups of guinea pigs were sensitized subconjunctivally with antiserum rich in IgG1 anti-DNP antibodies in both eyes (group 1, n = 11) or in one eye (group 2, n = 9; group 3, n = 10). The contralateral eyes of animals in groups 2 and 3 received normal guinea pig serum. At 1-hour intervals, beginning 6 h prior to challenge, guinea pigs in group 1 received 0.1% Dex in 0.5% hydroxymethylcellulose (MC) topically in one eye and 0.5% MC in their other eye. Animals in group 2 were treated on the same schedule with 0.5% MC only in both eyes. Animals in group 3 were not pretreated. Conjunctival edema, conjunctival erythema, periorbital swelling, and lid erythema were scored independently in the upper and lower lids of both eyes of all animals for 10 h. Comparisons between the scores of Dex-pretreated eyes in group 1 and MC-pretreated eyes in group 2 or untreated eyes in group 3 revealed no significant differences in any clinical sign at 0.5 h (early-phase reaction). However, these comparisons demonstrated significant reductions in all four clinical signs in animals of groups 1 from 1 to 8 h and marked reduction or complete absence of signs from 6 to 10 h (late-phase reaction).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Topical↗