Biomedical subjects

R Garofalo

Publications and source records attributed to R Garofalo.

At least 37 records · Page 2Linked to original sources

PubMed1998

Evolution of immunologic functions of the mammary gland and the postnatal development of immunity.

Physiologic delays in production of immune factors occur in mammals including Homo sapiens. This finding is counter to a basic tenet of biologic evolution, because such delays increase the risk of infections. The disadvantage is, however, offset by defense factors in milk of the species in whom the developmental delay occurs. Reciprocal relationships between the production of immune factors by the lactating mammary gland and the production of those defense agents during early infancy are found in all investigated mammalian species. Thus, the evolution of these processes is closely related. Certain immunologic components of milk are highly conserved, whereas others vary according to the species. The variations most likely evolved by genetic mutations and natural selection. In addition, the immune composition of mammalian milks is associated with developmental delays in the same immunologic agents. Furthermore, most closely related mammals, such as humans and chimpanzees, are most similar in the defense agents in their milks and the corresponding developmental delays in their immune systems. Defense factors in human milk include antimicrobial agents (secretory IgA, lactoferrin, lysozyme, glycoconjugates, oligosaccharides, and digestive products of milk lipids), antiinflammatory factors (antioxidants, epithelial growth factors, cellular protective agents, and enzymes that degrade mediators of inflammation), immunomodulators (nucleotides, cytokines, and antiidiotypic antibodies), and leukocytes (neutrophils, macrophages, and lymphocytes). Because of a lack of geographic/ethnic variation in the immunologic composition of human milk and corresponding immunologic delays in infants, these evolutionary processes seem stable. This is supported by investigations of diverse populations that indicate that this evolutionary outcome is highly beneficial to human infants.

Animals↗

PubMed1998

The association between health risk behaviors and sexual orientation among a school-based sample of adolescents.

OBJECTIVE: This study is one of the first to examine the association between sexual orientation and health risk behaviors among a representative, school-based sample of adolescents. DESIGN: This study was conducted on an anonymous, representative sample of 4159 9th- to 12th-grade students in public high schools from Massachusetts' expanded Centers for Disease Control and Prevention 1995 Youth Risk Behavior Survey. Sexual orientation was determined by the following question: "Which of the following best describes you?" A total of 104 students self-identified as gay, lesbian, or bisexual (GLB), representing 2.5% of the overall population. Of GLB youth, 66.7% were male and 70% were white (not Hispanic). Health risk and problem behaviors were analyzed comparing GLB youth and their peers. Those variables found to be significantly associated with GLB youth were then analyzed by multiple logistic regression models. RESULTS: GLB youth were more likely than their peers to have been victimized and threatened and to have been engaged in a variety of risk behaviors including suicidal ideation and attempts, multiple substance use, and sexual risk behaviors. Four separate logistic regression models were constructed. Model I, Onset of Behaviors Before Age 13, showed use of cocaine before age 13 years as strongly associated with GLB orientation (odds ratio [OR]: 6.10; 95% confidence interval [CI] = 2.45-15.20). Early initiation of sexual intercourse (2.15; 10.6-4.38), marijuana use (1.98; 1.04-4.09), and alcohol use (1.82; 1.03-3.23) also was associated with GLB orientation. Model II, Lifetime Frequencies of Behaviors, showed that frequency of crack cocaine use (1.38; 1.06-1.79), inhalant use (1.30; 1.05-1.61), and number of sexual partners (1.27; 1.06-1.43) was associated with GLB orientation. Model III, Frequency of Recent Behaviors, showed smokeless tobacco use in the past 30 days (1.38; 1. 20-1.59) and number of sexual partners in the previous 3 months (1. 47; 1.31-1.65) were associated with GLB orientation. Model IV, Frequency of Behaviors at School, showed having one's property stolen or deliberately damaged (1.23; 1.08-1.40) and using marijuana (1.29; 1.05-1.59) and smokeless tobacco (1.53; 1.30-1.81) were associated with GLB orientation. Overall, GLB respondents engaged disproportionately in multiple risk behaviors, reporting an increased mean number of risk behaviors (mean = 6.81 +/- 4.49) compared with the overall student population (mean = 3.45 +/- 3.15). CONCLUSION: GLB youth who self-identify during high school report disproportionate risk for a variety of health risk and problem behaviors, including suicide, victimization, sexual risk behaviors, and multiple substance use. In addition, these youth are more likely to report engaging in multiple risk behaviors and initiating risk behaviors at an earlier age than are their peers. These findings suggest that educational efforts, prevention programs, and health services must be designed to address the unique needs of GLB youth.

Adolescent↗

PubMed1997

Respiratory syncytial virus induces selective production of the chemokine RANTES by upper airway epithelial cells.

The presence of histamine and eosinophil cationic protein in nasopharyngeal secretions of infants with respiratory syncytial virus (RSV)-induced bronchiolitis implies the activation of basophil and eosinophil leukocytes, but the specific mechanism of their recruitment has not been elucidated. Chemokines are potent and selective leukocyte chemotactic molecules that are also expressed by airway epithelial cells. Therefore, the pattern of chemokines produced in response to RSV infection was investigated in primary cultures of human nose- and adenoid-derived epithelial cells. Interleukin-8, growth-related peptide-alpha, and monocyte chemotactic protein-1 were constitutively released by uninfected epithelial cells and were not further enhanced by infection with RSV. RANTES (regulated upon activation, normal T cell-expressed and -secreted), which was present in negligible concentrations in uninfected cultures, was strongly induced by RSV infection, in a dose- and time-dependent manner. Through the release of RANTES, epithelial cells may control the selective concentration and activation of basophils and eosinophils in RSV-infected airway mucosa.

Adenoids↗

PubMed1997

Differential stimulation of interleukin-12 (IL-12) and IL-10 by live and killed Helicobacter pylori in vitro and association of IL-12 production with gamma interferon-producing T cells in the human gastric mucosa.

The objective of these experiments was to examine the ability of Helicobacter pylori to stimulate interleukin-10 (IL-10) or IL-12 and select for either Th1 or Th2 cells. Gastric biopsy specimens were collected from patients who were categorized with respect to the presence of H. pylori and gastric disease as well as their age, gender, medications, and other factors. As Th1 and Th2 cells are selected by IL-12 and IL-10, respectively, biopsy specimens were screened for mRNA and protein for these cytokines. Although mRNA for IL-12 and IL-10 was detected in biopsy specimens obtained from both infected and uninfected patients, IL-12 protein predominated. Levels of IL-10 and IL-12 in gastric tissue did not change in response to infection. Moreover, gamma interferon (IFN-gamma)-producing T cells were found in both the infected and the uninfected gastric mucosa. Stimulation of peripheral blood leukocytes from either infected or uninfected donors with various concentrations of live or killed H. pylori induced immunoreactive IL-12 and IL-10. After stimulation with live H. pylori, IL-12 levels increased more than 30-fold, whereas IL-10 levels increased only 2- to 5-fold, compared to cells stimulated with medium alone. Interestingly, killed H. pylori induced significantly more IL-10 (P < 0.05) than live H. pylori, while recombinant urease only induced IL-10. These results demonstrate that live H. pylori selectively stimulates the induction of IL-12 and Th1 cells that produce IFN-gamma, whereas preparations used in oral vaccines induce more IL-10 and may favor Th2 cell responses.

Adult↗

PubMed1997

Antigen presentation of mucosal pathogens: the players and the rules.

A vast number of infectious pathogens gain entry into the host through mucosal surfaces, which have a much greater total surface area than the skin. Since the mucosa is continuously exposed to those pathogens, the development of an effective local immune response is of utmost importance. An obligatory step in the development of most immune responses is the presentation of antigens by specialized accessory cells, termed antigen-presenting cells (APC) to T lymphocytes. The recognition of antigens by T cells is largely determined by how the antigens are handled by the APC. Complex antigen-processing events generate a selected set of peptides which ultimately become associated with MHC molecules. The type of MHC molecules that bind the peptides in turn determine what T lymphocyte subset recognizes the peptides. Thus, an understanding of the molecular and cellular processes preceding the T cell recognition event is a prerequisite for understanding how mucosal immune responses develop, as well as for investigating alternative approaches to vaccine development and therapeutic strategies to control autoimmune diseases. This review discusses the cell biology of antigen processing and how various APC populations may participate in mucosal responses.

Animals↗

PubMed1996

Respiratory syncytial virus infection of human respiratory epithelial cells up-regulates class I MHC expression through the induction of IFN-beta and IL-1 alpha.

CD8+ T cells mediate some of the damage to the lung epithelium following respiratory syncytial virus (RSV) infection. Since CD8+ T cells recognize antigen-laden class I MHC molecules on the target cells, we examined in this study the expression of class I MHC by RSV-infected respiratory epithelial cells. Respiratory epithelial cell lines and bronchial epithelial cells from normal human tissue responded to RSV infection with an increased expression of class I MHC as determined by flow cytometry and immunoprecipitation of class I MHC from metabolically radiolabeled cells. The increase in class I MHC expression was dependent on infectious, replicating virus. UV-irradiated culture supernatants from RSV-infected A549 cells, when added to fresh A549 cell cultures, induced an increase in class I MHC expression by those cells. The class I MHC increasing activity within supernatants from A549 cells was due, in large part, to IFN-beta, and to a lesser extent to IL-1 alpha. The addition of neutralizing Abs to both cytokines completely blocked the increase in class I MHC expression by cells treated with the above-mentioned supernatants. These results demonstrate that RSV infection elicits IFN-beta production by respiratory epithelial cells, which in turn leads to an increase in their synthesis of class I MHC, which would facilitate their recognition and lysis by RSV-specific CD8+ T cells.

Adjuvants, Immunologic↗

PubMed1996

Cytokines in human milk: properties and potential effects upon the mammary gland and the neonate.

Epidemiologic and immunologic studies of breastfed and nonbreastfed infants and investigations of certain biologic activities in human milk led to the identification of immunomodulating agents in human milk. Among them were the cytokines interleukin-1 beta (IL-1 beta); IL-6, IL-8, IL-10, granulocyte-colony stimulating factor, macrophage-colony stimulating factor (M-CSF), tumor necrosis factor-alpha, interferon-gamma, epithelial growth factor (EGF), transforming growth factor-alpha (TGF-alpha), and TGF-beta 2. Interferon-gamma may originate from T cells in milk; EGF, TGF-alpha, TGF-beta, M-CSF, IL-6, and IL-8 may be produced by mammary gland epithelium. Based upon their known functions, we hypothesize that cytokines influence the development and immunologic function of the mammary gland and the neonate. Those in vivo functions remain to be defined by future investigations.

Adjuvants, Immunologic↗

PubMed1996

An ultrastructural study of the interaction of human eosinophils with respiratory syncytial virus.

It was shown previously that eosinophils are activated in vivo and in vitro by respiratory syncytial virus (RSV) (Garofalo et al., J Pediatr 1992: 120: 28-32; Kimpen et al., Pediatr Res 1992: 32: 160-4). For study of the interaction of eosinophils and RSV on the ultrastructural level, normodense eosinophils were purified from peripheral blood of healthy human volunteers. After incubation with RSV in the presence or absence of autologous serum, the eosinophils were examined with immunofluorescence microscopy employing an RSV-specific monoclonal antibody, and with transmission electron microscopy. After 2-h incubation in the presence of live RSV, 25.6 +/- 12.9% of the eosinophils demonstrated positive fluorescence. This increased to 62.8 +/- 8.9% when fresh autologous serum was added during incubation (P = 0.015). The effect was abolished when the serum was heat-treated, indicating Fc-receptor-independent enhancement of viral uptake by the cells. In transmission electron microscopy, virions were seen in phagocytic vacuoles at the periphery of the cells. Eosinophil activation characterized by piece-meal degranulation was evident. In conclusion, activation of eosinophils during RSV bronchiolitis probably occurs in part by direct interaction of the cells with the virus.

Adult↗

PubMed1996

Transcriptional activation of the interleukin-8 gene by respiratory syncytial virus infection in alveolar epithelial cells: nuclear translocation of the RelA transcription factor as a mechanism producing airway mucosal inflammation.

The most common cause of epidemic pediatric respiratory disease, respiratory syncytial virus (RSV), stimulates interleukin-8 (IL-8) synthesis upon infecting airway epithelium, an event necessary for the development of mucosal inflammation. We investigated the mechanism for enhanced IL-8 production in human A549 type II pulmonary epithelial cells. Infection with sucrose-purified RSV (pRSV) produced a time-dependent increase in the transcriptional initiation rate of the IL-8 gene. Transient transfection of the human IL-8 promoter mutated in the binding site for nuclear factor-kappaB (NF-kappaB) demonstrated that this sequence was essential for pRSV-activated transcription. Gel mobility shift assays demonstrated pRSV induction of sequence-specific binding complexes; these complexes were supershifted only by antibodies directed to the potent NF-kappaB transactivating subunit RelA. Both Western immunoblot and indirect immunofluorescence assays showed that cytoplasmic RelA in uninfected cells became localized to the nucleus after pRSV infection. RelA activation requires replicating RSV, because neither conditioned medium nor UV-inactivated pRSV was able to stimulate its translocation. We conclude that RelA undergoes changes in subcellular distribution in airway epithelial cells upon pRSV infection. The ability of replicating RSV to activate RelA translocation may play an important role in activating IL-8 and other inflammatory gene products necessary for airway mucosal inflammation seen in RSV disease.

Cell Nucleus↗

PubMed1996

Inducible translational regulation of the NF-IL6 transcription factor by respiratory syncytial virus infection in pulmonary epithelial cells.

Respiratory syncytial virus (RSV), the most common etiologic agent of epidemic pediatric respiratory disease, infects and replicates in the human airway epithelium, resulting in the induction of cellular gene products essential for immune and inflammatory responses. We describe the effect of RSV infection on nuclear factor-IL6 (NF-IL6) expression, a human basic domain-leucine zipper-containing transcription factor that alone in combination with other inducible transcription factors regulates the expression of cytokine and adhesion molecule genes. RSV-infected human type II pulmonary alveolar epithelial cells (A549) synthesize a single 45.7-kDa isoform of NF-IL6 rapidly and in a time-dependent manner. NF-IL6 is first detectable after 3 h of infection and continues to accumulate until 48 h (until the cells lose viability). NF-IL6 production could not be induced by UV-inactivated virus, demonstrating the requirement of viral replication for NF-IL6 synthesis. Immunoprecipitation after [35S]methionine metabolic labeling was done to investigate the mechanism for NF-IL6 production. There was robust NF-IL6 protein synthesis within RSV-infected (24 h) cells. Protein synthesis occurred without detectable changes in the abundance or size of the single 1.8-kb NF-IL6 mRNA. RNase protection assay of transfected chloramphenicol acetyltransferase reporter genes driven by either wild-type or mutated NF-IL6 binding sites show a virus-induced increase in NF-IL6-dependent transcription. These studies have demonstrated a novel inducible mechanism for translational control of NF-IL6 synthesis and identify this transcription factor as a potential effector of the host response to RSV infection.

Base Sequence↗

PubMed1996

Role of leukotriene B4 and interleukin-8 in acute bacterial and viral otitis media.

In order to evaluate the role of polymorphonuclear leukocytes (PMNs) in acute otitis media (AOM), levels of leukotriene B4 (LTB4), a potent inflammatory product of PMNs, and interleukin-8 (IL-8), a PMN chemotactic cytokine, were measured in 271 middle ear fluid (MEF) samples from 106 children with AOM. Forty-two percent of the patients had evidence of respiratory viral infection. At the time of diagnosis, levels of both LTB4 and IL-8 were higher in the MEFs from patients with AOM associated with bacterial or bacterial and viral infection than those MEFs containing no pathogen (p < .05). Antibiotic treatment was not associated with a significant change in levels of LTB4 or IL-8 in the MEFs obtained 2 to 5 days into treatment, compared to those obtained at diagnosis. Bacteriologic failure after 2 to 5 days of treatment was associated with high LTB4 levels in the initial MEFs (p = .05). Recurrence of AOM within 1 month was associated with high IL-8 levels in the initial MEF (p = .04). Our findings suggest that LTB4 and IL-8 are produced during acute infection of the middle ear, and these PMN-related inflammatory substances may play an important role in delaying recovery or in recurrence of AOM. Effective treatment of AOM may require eradication of bacteria by antibiotics, as well as pharmacologic agents that modulate PMN functions.

Bacterial Infections↗

PubMed1996

Decreased interleukin-10 production by neonatal monocytes and T cells: relationship to decreased production and expression of tumor necrosis factor-alpha and its receptors.

The production of IL-10 by human neonatal blood mononuclear leukocytes (BML) stimulated with lipopolysaccharide (LPS), tumor necrosis factor-alpha (TNF-alpha), antibodies to CD3, or phorbol 12-myristate 13-acetate (PMA) was measured. The production of IL-10 by neonatal BML cultured with LPS or TNF-alpha was approximately 20 and approximately 15%, respectively, of adult BML. The combination of human recombinant TNF-alpha and LPS failed to augment IL-10 production in neonatal BML. The decreased production of IL-10 by neonatal leukocytes was not due to an autocrine feedback mechanism because only low concentrations of IL-10 were found in newborn sera. A connection with TNF-alpha could not be ruled out, because TNF-alpha production by LPS-stimulated newborn BML and the expression of TNF-alpha receptors on newborn monocytes were reduced. Mean +/- SD of concentrations of IL-10 in supernatants from adult and neonatal BML after stimulation with antibodies to human CD3 for 48 or 72 h were 914 +/- 386 and 178 +/- 176 pg/mL, respectively (p < 0.0001). In experiments with enriched populations of neonatal T cells, the addition of PMA failed to augment IL-10 production. This suggested that newborn T cells may be in a different state of activation than adult T cells Thus, IL-10 production in neonatal monocytes and T cells is reduced and this study suggests that the reduction may be secondary in part to regulatory processes involving TNF-alpha and its receptors.

Adolescent↗

PubMed1995

Differences in the acute actions of sGnRH and cGnRH-II on gonadotropin release in goldfish pituitary cells.

The signal transduction mechanisms mediating the acute actions of salmon gonadotropin (GTH)-releasing hormone (sGnRH) and chicken GnRH-II (cGnRH-II) on GTH release from goldfish pituitary cells were compared. In cell column perifusion experiments, treatment with inhibitors of phospholipase A2 (50 microM quinacrine or 50 microM bromophenacylbromide) or the lipoxygenase enzyme (50 microM nordihydroguaiaretic acid) reduced the GTH response to 100 nM sGnRH, but not the response to 100 nM cGnRH-II. These results suggest that AA mobilization through phospholipase A2 and the subsequent metabolism of AA through the lipoxygenase pathway are involved in rapid sGnRH-induced GTH secretion, but not in acute cGnRH-II action. Consistent with the idea that calcium entry through voltage-sensitive calcium channels is involved in acute GnRH action, perfusion with 1 microM verapamil, a voltage-sensitive calcium channel inhibitor, reduced both 100 nM sGnRH- and 100 nM cGnRH-II-induced GTH secretion. However, the response to cGnRH-II was decreased to a greater extent compared to sGnRH-elicited release, suggesting a greater dependence on extracellular calcium entry for acute cGnRH-II-stimulated GTH secretion. The metabolism of inositol phosphates (InsPs) following acute sGnRH and cGnRH-II administration was also investigated by monitoring the levels of [3H]InsPs in [3H]inositol-prelabeled goldfish pituitary cells. Incubation with 100 nM sGnRH increased [3H]InsP1 by 5 min and [3H]InsP2, [3H]InsP3, and other higher [3H]InsPs by 10 min. In contrast, following 10 min of stimulation by 100 nM cGnRH-II, only [3H]InsP2 levels were elevated, suggesting that cGnRH-II may activate a different set of enzymes in the phosphoinositide metabolic pathways compared to sGnRH. The lack of an InsP3 response may also reflect the relative ineffectiveness of cGnRH-II to mobilize calcium from intracellular stores. Taken together, these results strongly indicate that the mechanisms mediating rapid sGnRH-induced and cGnRH-II-elicited GTH responses are different as in the case for prolonged GnRH action.

Acetophenones↗

PubMed1995

Interleukin-1 alpha mediates the enhanced expression of intercellular adhesion molecule-1 in pulmonary epithelial cells infected with respiratory syncytial virus.

The mechanisms of virus-induced enhancement of intercellular adhesion molecule-1 (ICAM-1) expression in epithelial cells are unknown. In the present study, the effect of respiratory syncytial virus (RSV) infection on the expression of ICAM-1 in human pulmonary type II-like epithelial (A549) cells was evaluated. Conditioned RSV media (cRSV) produced from growth of RSV in A549 cells induced a significant increase in the expression of ICAM-1. Treatment of the cells with noninfectious cRSV prepared by ultraviolet (UV) irradiation (UV-cRSV) or ribavirin treatment resulted in the expression of ICAM-1 to a similar extent as infectious cRSV. These results suggested that RSV induces the synthesis of a soluble mediator(s) that regulates the expression of ICAM-1. Cytokine analysis by immunoassay and polymerase chain reaction showed that RSV induces the synthesis of interleukin (IL)-1 alpha and -beta, and tumor necrosis factor alpha (TNF-alpha). Preincubation of UV-cRSV with soluble IL-1 receptor (sIL-1r) almost completely blocked the enhancement of ICAM-1 expression. Furthermore, simultaneous incubation of infectious purified RSV with sIL-1r resulted in a significant reduction in enhancement of ICAM-1 expression. Preincubation with neutralizing antibodies to IL-1 alpha and -beta, and TNF-alpha showed that the predominant ICAM-1 enhancing soluble mediator in UV-cRSV was IL-1 alpha. These experiments provide direct evidence for an autocrine mechanism of enhanced ICAM-1 expression in RSV-infected epithelial cells that is mediated primarily by IL-1 alpha. Pulmonary epithelial cells may play an important immunoregulatory role in the microenvironment of the lower respiratory tract infected with RSV.

Cell Adhesion↗

PubMed1995

Interleukin-10 in human milk.

The concentrations of immunoreactive IL-10 in the aqueous fraction of 20 specimens of human milk obtained during the first 80 h of lactation and stored at -60 degrees C ranged from 66 to 9301 pg/mL (mean +/- SD, 3304 +/- 3127 pg/mL). IL-10 was present also in the lipid layer of milk. Gel filtration revealed that IL-10 was located in a high molecular weight fraction, where certain other cytokines in human milk have been found. In addition, immunoreactive IL-10 in milk increased after treatment with sodium taurocholate. Bioactive IL-10 was demonstrated by the finding that human milk inhibited [3H]thymidine uptake by human blood lymphocytes and that inhibition was partly overcome by concomitant incubation with antibodies to human IL-10. IL-10 mRNA but no protein product was found in cultured human mammary epithelial cells. Some IL-10 was associated with preparations of human milk leukocytes, but the data did not suggest that the cells were producing the cytokine. Bioactive IL-10 in a possible protected compartment suggests that IL-10 in human milk may have immunomodulating, antiinflammatory effects on the alimentary tract of the recipient infant.

Adult↗

PubMed1994

Production of interleukin-6 and interleukin-8 by human mammary gland epithelial cells.

The production of transforming growth factor-beta 2 (TGF-beta 2), interleukin-1 beta (IL-1 beta), IL-6, IL-8, and tumor necrosis factor-alpha (TNF-alpha) by spontaneously immortalized human mammary gland epithelial cells of non-malignant origin and the effect of prolactin upon the production of those cytokines were investigated. Cells were cultured on plastic with epithelial growth factor, insulin, and hydrocortisone. Cytokines were quantified by enzyme-immunoassays. The cells produced IL-6 and IL-8, but no detectable TGF-beta 2, IL-1 beta, or TNF-alpha. Although prolactin enhanced the uptake of [3H]thymidine, it did not alter the production of cytokines/interleukins. Because of the marked production of IL-8 by mammary epithelium and a past report of TGF activity in human milk, those agents were quantified in human milk. The mean +/- S.D. concentrations of IL-8 and TGF-beta 2 in human milk obtained in the first 3 days of lactation were 3684 +/- 2910 and 130 +/- 108 pg/ml, respectively. Thus, IL-8 and TGF-beta 2 are normal constituents in human milk, and human mammary gland epithelium may be responsible for producing some of the IL-6 and IL-8 in human milk.

Adult↗

PubMed1994

Virus and bacteria enhance histamine production in middle ear fluids of children with acute otitis media.

Histamine levels were measured in 677 middle ear fluid (MEF) samples from 248 children (aged 2 months to 7 years) with acute otitis media (AOM); of these, 116 (47%) had documented viral infection. Histamine content was higher in bacteria-positive than in bacteria-negative MEF samples (P = .007) and higher in samples from patients with viral infection than in those from patients with no viral infection (P = .002). Bacteria and viruses together had an additive effect on histamine content in MEF. Histamine concentration in the initial MEF sample tended to be higher in patients with persistent otitis than in those with good response to treatment (P = .14). Results suggest that viruses, bacteria, or both induce histamine production, which leads to increased inflammation in the middle ear. Antihistaminic drugs may be beneficial. Large, prospective, controlled trials of the effects of antihistamine as an adjunct therapy in bacterial and viral AOM are required before recommendations can be made.

Acute Disease↗

PubMed1994

Peripheral blood eosinophil counts and eosinophil cationic protein content of respiratory secretions in bronchiolitis: relationship to severity of disease.

Infants and young children with acute viral respiratory illness were studied to determine the association of peripheral blood eosinophil counts and concentrations of eosinophil cationic protein (ECP) in nasopharyngeal secretions with the development and severity of bronchiolitis. Subjects included those with upper respiratory illness (URI) alone, pneumonia or bronchiolitis. Controls consisted of healthy infants, and those hospitalized with non-respiratory illnesses. While peripheral blood eosinophil counts were suppressed in all infected infants greater than two months of age, eosinophil counts in patients with bronchiolitis were significantly greater than in those with URI alone. ECP concentrations were significantly greater among individuals with bronchiolitis than other infected infants. For bronchiolitis cases with detectable peripheral blood eosinophils, eosinophil counts correlated weakly and inversely with oxygen saturations. In contrast, ECP concentrations were strongly inversely correlated with initial oxygen saturation. ECP concentrations were also significantly correlated with peripheral blood eosinophil counts. Viral infections suppress peripheral blood eosinophil counts in infants greater than two months of age, although the effect is somewhat overcome in patients with bronchiolitis. The form and severity of bronchiolitis is much more strongly related to degranulation of eosinophils in the respiratory tract than to peripheral blood eosinophil counts.

Blood Proteins↗