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PubMed2000

Modulation of nitric oxide synthesis in inflammation. Relationship to oxygen-derived free radicals and prostaglandin synthesis.

The role of nitric oxide (NO) derived from constitutive (cNOS) and inducible (iNOS) nitric oxide synthases and its relationship to oxygen-derived free radicals and prostaglandins was investigated in two models of inflammation, namely, carrageenan granuloma air pouch (acute model) and Freund's adjuvant-induced arthritis (chronic model) in rats. Inflammation was assessed by measurement of NO and prostaglandin E2 (PGE2) levels and the lysosomal leakage of the enzyme N-acetyl-B-D-glucosaminidase (NAG) into the exudate of the granuloma pouch 4 h after carrageenan injection. Evaluation of paw volume and determination of serum NO, lipid peroxide (LP), and PGE2 levels were used for the assessment of adjuvant-induced arthritis after either 4 days (early phase) or 16 days (late phase) of adjuvant injection. Results of the study showed that the administration of either NG-nitro-L-arginine methyl ester (L-NAME, non-selective cNOS/iNOS inhibitor) or aminoguanidine (AG, selective iNOS inhibitor), prior to carrageenan injection or during development of adjuvant arthritis, caused a significant reduction in NO and PGE2 levels and in the NAG activity of the granuloma inflammatory exudate, whereas decreases in paw volume and in serum NO level were noticed in the adjuvant model as related to untreated rats. Similar treatment with L-arginine failed to elaborate a significant change in the parameters measured. Other observations included: no noticeable differences between the results of early and late phases of adjuvant arthritis; no clear correlation between NO, LP and PGE2 levels in the adjuvant arthritis inflammation and inability of the NOS inhibitors to modify the levels of serum LP that is increased during adjuvant-induced arthritis. The data give further evidence that NO is implicated in the development of both acute and chronic inflammation and that NOS inhibitors have potential antiinflammatory activity. Further studies are required to unravel the mechanisms by which NO interacts with other mediators of inflammation.

Acetylglucosaminidase↗
PubMed2005

Influence of systemic inflammation on the interpretation of response to antiplatelet therapy, monitored by PFA-100.

Recently it was shown that inflammation adversely influences results obtained with the Platelet Function Analyzer System PFA-100, hypothesizing that inflammation could confound interpretation of platelet function results. We investigated the clinical relevance of these results in patients with peripheral arterial occlusive disease (PAOD), with and without signs of systemic inflammation. In 98 PAOD patients, all treated with acetylsalicylic acid (ASA), we measured PFA-100 closure times with the collagen-epinephrine test cartridges. C-reactive protein (CRP) values were measured as an indicator for systemic inflammation. Mean CRP levels were elevated in 23 patients (23%). There was no difference in mean PFA-100 results between patients with elevated CRP-levels and those without. During clinical use of the PFA system, systemic inflammation had no major influence on the performance of the collagen-epinephrine cartridge. With respect to the response to antiplatelet therapy with ASA, the results suggest that the platelet inhibitory effect of ASA is not reduced under inflammatory conditions.

Arterial Occlusive Diseases↗
PubMed2006

Tissue factor in infection and severe inflammation.

In the pathogenesis of vascular disease, inflammation and coagulation play a pivotal role. Increasing evidence points to an extensive cross-talk between these two systems, whereby inflammation not only leads to activation of coagulation, but coagulation also considerably affects inflammatory activity. Tissue factor (TF) plays an important role at the crossroad of coagulation and inflammation, as the principal initiator of coagulation and an important modulator of inflammation. Proinflammatory cytokines can induce TF expression on mononuclear cells and endothelial cells and thereby commence pathways that lead to thrombin generation. Simultaneously, TF may bind to cellular receptors, which may affect the production and release of inflammatory mediators. There is increasing experimental evidence that TF inhibition may have beneficial effects in disease states in which the combination of coagulation and inflammation plays a prominent role.

Blood Coagulation↗
PubMed2007

The role of inflammation and infection in preterm birth.

Inflammation has been implicated in the mechanisms responsible for preterm and term parturition, as well as fetal injury. Out of all of the suspected causes of preterm labor and delivery, infection and/or inflammation is the only pathological process for which both a firm causal link with preterm birth has been established and a molecular pathophysiology defined. Inflammation has also been implicated in the mechanism of spontaneous parturition at term. Most cases of histopathological inflammation and histological chorioamnionitis, both in preterm and term labor, are sub-clinical in nature. The isolation of bacteria in the amniotic fluid, known as microbial invasion of the amniotic cavity, is a pathological finding; the frequency of which is dependent upon the clinical presentation and gestational age. This article reviews the role of inflammation in preterm and term parturition.

Amnion↗
PubMed2001

L-Selectin is required for the development of airway hyperresponsiveness but not airway inflammation in a murine model of asthma.

BACKGROUND: Airway inflammation and airway hyperresponsiveness (AHR) are fundamental features of asthma. Migration of inflammatory cells from the circulation into the lungs is dependent on adhesion molecule interactions. The cell surface adhesion molecule L-selectin has been demonstrated to mediate leukocyte rolling on inflamed and noninflamed pulmonary endothelium. However, its role in the development of airway inflammation and AHR in asthma has not been examined. OBJECTIVE: We sought to characterize the role of L-selectin in the recruitment of inflammatory cells to the airway-lung and the development of AHR in a murine model of asthma. METHODS: An ovalbumin (OVA)-induced allergic airway disease model of asthma was applied to L-selectin-deficient (LKO) mice and C57BL/6 wild-type (WT) control mice. The development of airway inflammation was assessed by examining leukocyte influx into bronchoalveolar lavage (BAL) fluid and the lung. Total and differential BAL leukocyte counts were determined, and the immunophenotype of BAL lymphocytes was assessed by means of flow cytometry. The development of AHR was assessed by means of whole-body plethysmography. RESULTS: Airway-lung inflammation was equivalent in LKO and WT mice sensitized-challenged with OVA, as measured by total and differential BAL cell counts and histologic analysis of lung tissue. Numbers of eosinophils, neutrophils, lymphocytes, and monocytes in BAL fluid were equivalent in LKO and WT mice. However, phenotypic analysis of BAL lymphocytes demonstrated significantly reduced CD3(+) populations and increased B220(+) populations in LKO compared with WT mice (P <.05). Remarkably, despite a fulminant inflammatory response in the airway-lung in LKO mice sensitized-challenged with OVA, AHR was completely abrogated. CONCLUSION: L-selectin plays a crucial role in the development of AHR but not allergic inflammation in an animal model of asthma. L-selectin represents a potential target for novel asthma therapies specifically aimed at controlling AHR.

Animals↗
PubMed2002

Therapeutic significance of distal airway inflammation in asthma.

Inflammation in asthma is not merely confined to the large central airways but also extends to the small peripheral airways. Distal lung inflammation can be observed even in patients with asthma with mild disease and normal spirometric readings. Subjects with asymptomatic asthma can exhibit significant increases in peripheral airway resistance, likely the result of distal lung inflammation. As determined from measurements of eosinophilic and other cellular infiltrates, the inflammatory response in the distal lung can exceed that in the large airways. Nocturnal asthma, a natural model of cyclic asthma worsening, is associated with an increase in nighttime distal lung inflammation, as evidenced by the accumulation of alveolar tissue eosinophils. Distal lung disease appears to increase the risk of recurrent asthma exacerbation, whereas disease-related anatomic changes in the small airways of the distal lung are prominent in fatal asthma. The clinical significance of distal lung disease makes this region an important therapeutic target. Chlorofluorocarbon (CFC)-based preparations of inhaled corticosteroids used to treat airway inflammation produce aerosols of relatively large particle size (approximately 4 microm); such aerosols have poor access to the distal lung. New formulations of inhaled corticosteroids that use hydrofluoroalkane (HFA) propellants can have smaller particle sizes (approximately 1 microm). Extrafine HFA aerosols have better access to the distal lung, with less oropharyngeal deposition. Imaging studies suggest that anti-inflammatory medication delivered as an extrafine aerosol produces beneficial changes in distal lung function. In one study, an HFA formulation of an inhaled corticosteroid reduced air trapping to a greater degree than a CFC formulation of the same corticosteroid. By extending the delivery of anti-inflammatory medication to the distal lung, the new HFA-based corticosteroids have the potential to treat asthma more effectively and at reduced steroid doses.

Aerosol Propellants↗
PubMed2002

Airway inflammation in asthma and its consequences: implications for treatment in children and adults.

The development and wide availability of novel research techniques such as bronchoscopy and induced sputum have enhanced our understanding of the pathophysiology of asthma. The appreciation of the inflammatory nature of asthma and the remodeling associated with chronic disease have undoubtedly led to improved disease management and a better understanding of how anti-asthma drugs work. Although extensive data about inflammation and its sequelae in children are lacking, both chronic inflammation and airway remodeling are more than likely to be involved in the development and progression of asthma in this young population. Indeed, evidence suggests that airway restructuring occurs early. The implications for treatment in any differences of inflammation and remodeling between children and adults, then, are likely to be important. Although corticosteroids are considered as first-line anti-inflammatory treatment, especially in chronic asthma, for many patients neither inhaled nor oral corticosteroid therapy can control inflammation adequately. In children, neither the addition of long-acting beta(2)-agonist therapy nor doubling of the corticosteroid dose has produced the same benefits seen in adults. A clearer understanding of the pathophysiologic mechanisms of asthma in adults and pediatric patients should provide new insights into different asthma phenotypes. Therefore, the development and application of relatively simple and safe methods for assessing markers of inflammation and alterations in the airways are vital, especially for children.

Adult↗
PubMed2001

Dense inflammation does not mask residual primary basal cell carcinoma during Mohs micrographic surgery.

BACKGROUND: Areas of dense inflammation are commonly removed during Mohs micrographic surgery for basal cell carcinoma because of the concern that they may mask areas of tumor. OBJECTIVE: Our purpose was to determine whether inflammation masks tumor during Mohs surgery for primary basal cell carcinoma. METHODS: Twenty-five consecutive cases of primary basal cell carcinoma with areas of dense inflammation encountered during Mohs surgery were sectioned and stained with hematoxylin and eosin and Ber-EP4. RESULTS: In no cases did the dense inflammation mask residual tumor. CONCLUSION: Dense inflammation does not mask primary basal cell carcinoma during Mohs surgery and should be carefully evaluated before additional surgery is performed.

Antibodies, Monoclonal↗
PubMed1997

Allergen-induced bronchial hyperreactivity and eosinophilic inflammation occur in the absence of IgE in a mouse model of asthma.

In patients with asthma, elevations of IgE correlate both with allergic inflammation of the airways and with bronchial hyperreactivity (BHR). Several investigations, using mouse models of this disease, have indicated a central role for IgE in the pathogenesis of the eosinophilic inflammation as well as in the obstructive airway physiology of BHR. Some diagnostic studies and therapeutic strategies for asthma are based on the putative role of IgE in asthma pathogenesis. Here, we use mice with a null mutation of the C epsilon locus to show that bronchial inflammation and BHR in response to allergen inhalation both can occur in the absence of IgE. We demonstrate that the eosinophilic bronchial inflammation elicited in an established mouse model of hypersensitivity to Aspergillus fumigatus (Af) is accompanied by the asthmatic physiology of BHR. Wild-type and IgE-deficient mice were sensitized intranasally with Af extract. Both groups of animals developed bronchoalveolar lavage eosinophilia and pulmonary parenchymal eosinophilia. This was accompanied by increased serum levels of total and Af-specific IgE in the wild-type animals only. This Af-sensitization protocol resulted in significant BHR in both wild-type mice and IgE-deficient mice. Interestingly, unsensitized IgE-deficient mice had increased bronchial responsiveness compared with unsensitized wild-type controls. We conclude that BHR and airways inflammation can be fully expressed via IgE-independent mechanisms. These may involve the activation of mast cells by factors other than IgE as well as a mucosal lymphocyte-mediated immune response to allergen.

Allergens↗
PubMed2002

Transgenic overexpression of interleukin (IL)-10 in the lung causes mucus metaplasia, tissue inflammation, and airway remodeling via IL-13-dependent and -independent pathways.

To address the complex chronic effector properties of interleukin (IL)-10, we generated transgenic mice in which IL-10 was overexpressed in the lung. In these mice, IL-10 inhibited endotoxin-induced tumor necrosis factor production and neutrophil accumulation. IL-10 also caused mucus metaplasia, B and T cell-rich inflammation, and subepithelial fibrosis and augmented the levels of mRNA encoding Gob-5, mucins, and IL-13. In mice bred to have null mutations of IL-13, IL-4R(alpha), or STAT-6, transgenic IL-10 did not induce mucus metaplasia but did induce inflammation and fibrosis. IL-10 was also a critical mucin regulator of virus-induced mucus metaplasia. Thus, IL-10, although inhibiting lipopolysaccharide-induced inflammation, also causes mucus metaplasia, tissue inflammation, and airway fibrosis. These responses are mediated by multiple mechanisms with mucus metaplasia being dependent on and the inflammation and fibrosis being independent of an IL-13/IL-4R(alpha)/STAT-6 activation pathway.

Animals↗
PubMed2003

5-Chlorouracil, a marker of DNA damage from hypochlorous acid during inflammation. A gas chromatography-mass spectrometry assay.

Hypochlorous acid (HOCl), generated from H2O2 and Cl- by myeloperoxidase in activated neutrophils, causes tissue damage during inflammation. We have developed a simple, sensitive (approximately 0.2 fmol on column) and specific GC-MS assay for the detection of 5-chlorouracil (5-ClUra), a signature product of HOCl-mediated damage to nucleobases. In this assay, 5-ClUra is released from isolated DNA by a digestion with nuclease P1, alkaline phosphatase, and thymidine phosphorylase (TP), or from chlorinated nucleosides in biological fluids by TP. The freed 5-ClUra is derivatized with 3, 5-bis-(trifluoromethyl)-benzyl bromide, which is detected by negative chemical ionization mass spectrometry. The assay can be used to simultaneously detect other halogenated uracils including bromouracil. Using this assay, we showed that 5-ClUra is generated by the reaction of low micromolar HOCl with (deoxy)cytidine, (deoxy)uridine, and DNA. In cell cultures, an increase of 5-ClUra was detected in DNA when cells were treated with sublethal doses of HOCl and allowed to proliferate. The elevation of 5-ClUra was markedly accentuated when physiologically relevant concentrations of (deoxy)uridine, (deoxy) cytidine, uracil, or cytosine were present in the medium during HOCl treatment. In the carrageenan-induced inflammation model in rats, chlorinated nucleosides was significantly increased, compared with controls, in the exudate fluid isolated from the inflammation site. Our study provides the direct evidence that chlorinated nucleosides are found in the inflammation site and can be incorporated in DNA during cell/tissue proliferation. These findings may be relevant to the carcinogenesis associated with chronic inflammation.

Alkaline Phosphatase↗
PubMed2002

Mast cells involvement in the inflammation and fibrosis development of the TNBS-induced rat model of colitis.

BACKGROUND: Mast cells have been implicated in chronic inflammatory conditions resulting in fibrosis, such as Crohn disease. However, a link between inflammation, fibrosis and mast cells has not been demonstrated in human or animal intestinal diseases. This work was undertaken to analyze whether mast cells play a role in inflammation and fibrosis in the TNBS-induced rat colitis. METHODS: Rats were rectally instilled 2,4,6,-trinitrobenzene sulfonic acid in ethanol, and immediately or 4 days later injected daily i.p. with nedocromil sodium, a mast cell stabilizer, compound 48/80, a mast cell activator, or saline. Rats were sacrificed 5 days post-TNBS, or on day 21. Intestinal inflammation and fibrosis were assessed by gross and histopathological evaluation. Colonic mast cell numbers (toluidine blue) and collagen (type I mRNA expression) were evaluated. Mast cell sonicate was added to rat colon fibroblasts. Fibroblast proliferation (3H-thymidine), collagen synthesis (3H-proline) and contractile activity (tridimensional collagen lattice contraction) were then assessed. RESULTS: Nedocromil reduced inflammation and fibrosis possibly by decreasing mast cell numbers and activation and consequent collagen production. Compound 48/80 slightly enhanced the severity of the disease by activating mast cells. Mast cells increased fibroblast proliferation, collagen production and contractile activity. CONCLUSIONS: Mast cells are involved in the gastrointestinal tract inflammation and fibrosis of the TNBS-colitis rats.

Animals↗
PubMed2000

Using serum amyloid A to screen dairy cows for sub-clinical inflammation.

In this study, 232 lactating dairy cows from six herds were observed for clinical signs of inflammation and simultaneously had blood samples drawn to determine whether or not Serum Amyloid A (SAA) was present. Serum protein electrophoresis and white blood cell differential count revealed inflammation in SAA+ samples but not in SAA-samples. Using positive SAA test results as the standard for presence of inflammation, clinical findings consistent with inflammation concurred with positive SAA results only 26% of the time (p<.001) while the lack of clinical signs consistent with inflammation concurred with negative SAA results 95% of the time (p<.001). There was also a significant difference (p<.005) in management styles in that cows permanently fed on wilted/cured forages and kept inside had a 26% prevalence of positive SAA blood samples whereas the overall prevalence of SAA+ samples was 16%. These findings indicate that whole herd screening using SAA can be of value to the veterinarian in helping to identify cows with inflammatory diseases. From a public health perspective, SAA testing of cows going to market can help differentiate those not needing intensive inspection from those that do.

Acute-Phase Reaction↗
PubMed2006

Non-allergic eosinophilic inflammation.

Much is known about the eosinophilic processes associated with antigens, tumors, and infection, yet data on other causes of eosinophilic inflammation are scarce. This paper investigates the locations and causes of other nonrespiratory eosinophilic inflammation. Although eosinophilic inflammation can involve locomotor, urinary, cardiovascular, nervous, gastrointestinal, and other mucosal surfaces, such inflammation also can accompany tissue trauma, foreign-body reactions, and necrotic or granulomatous processes. Despite their cytolytic/histolytic effects, eosinophil leukocytes are a component of tissue remodeling, can be antigen-presenting cells, and have a role in the reproductive system and in blood coagulation. The study of various types of eosinophilic inflammation may increase our understanding of the biological responses of eosinophil leukocytes to different inflammatory stimuli.

Eosinophilia↗
PubMed2006

Malnutrition-inflammation-atherosclerosis (MIA) syndrome components in hemodialysis and peritoneal dialysis patients.

BACKGROUND: Malnutrition, inflammation, and atherosclerosis (MIA syndrome) are common in end-stage renal disease (ESRD) patients. Each component of MIA syndrome is the predictor of outcomes in ESRD patients. In this cross-sectional study, we aimed to compare both dialysis modalities for MIA syndrome components. MATERIAL AND METHODS: Thirty hemodialysis (HD) (mean age 44 +/- 11 years, 14 male and 16 female, mean time on dialysis: 31.0 +/- 19.0 months) and 30 continuous ambulatory peritoneal dialysis (CAPD) patients (41 +/- 9 years, 12 male and 18 female, mean time on dialysis: 25.5 +/- 21.5 months) were included. In order to determine malnutrition in ESRD patients, serum albumin level and anthropometric measurements were used. For inflammation, serum C-reactive protein level, erythrocyte sedimentation rate, and fibrinogen levels were measured. Mean-carotid artery intima media thickness (m-CIMT), presence of carotid plaque and serum homocysteine level were used to determine atherosclerosis. RESULTS: Five CAPD patients (16%) and one HD patient (3%) was hypoalbuminemic. HD and CAPD groups were similar for inflammation. Mean-CIMT and serum homocysteine level were higher in HD patients than CAPD patients. There was a positive correlation between homocysteine and m-CIMT. CONCLUSION: Before choosing renal replacement therapy, malnutrition, inflammation, and atherosclerosis parameters must be investigated in ESRD patients. Hemodialysis seems to be more advantageous for malnutrition components than CAPD. Both dialysis modalities seem to be similar for inflammation, and CAPD modality has superiority for atherosclerosis. Before choosing the type of renal replacement therapy, assessment of MIA syndrome components could be useful for individualization of the decision on which dialytic modality is appropriate in ESRD patients.

Adult↗
PubMed2000

Protection against ozone-induced pulmonary inflammation and cell death by endotoxin pretreatment in mice: role of HO-1.

Ozone is a ubiquitous air pollutant that can cause acute pulmonary inflammation and cell injury and may contribute to the exacerbation of chronic pulmonary diseases. The molecular mechanisms of ozone-induced cell injury, as well as protective mechanisms against ozone-injury, are not well understood. Since ozone is a reactive oxidant, and heme oxygenase-1 (HO-1) is an antioxidant enzyme induced by many oxidative stimuli, we hypothesized that HO-1 is one of the protective mechanisms against ozone-induced cell injury, as well as pulmonary inflammation. In the current study, C57Bl/6 mice were pretreated with a low level of endotoxin (lipopolysaccharide, LPS) (0.5 mg/kg) to induce HO-1, and 16 h later were exposed to 1 ppm ozone for 3 h. Endotoxin pretreatment caused a significant protection against ozone-induced pulmonary inflammation and cell injury in bronchoalveolar lavage (BAL) cells. The protection by endotoxin pretreatment against ozone-induced inflammation and necrosis in BAL cells was abolished by the cotreatment with a heme oxygenase inhibitor, tin protoporphyrin IX dichloride (SnPP), suggesting that HO-1 is responsible for the protection against ozone-induced pulmonary inflammation and BAL cell necrosis. Therefore, since HO-1 is induced following ozone exposure, HO-1 may contribute to the development of cellular adaptation to chronic ozone exposure.

Animals↗
PubMed2005

Superoxide dismutase (SOD) as a potential inhibitory mediator of inflammation via neutrophil apoptosis.

Superoxide dismutase (SOD) is supposed to be an effective agent for neutrophil-mediated inflammation in the area of critical medicine. We investigated the involvement of SOD in the regulation of neutrophil apoptosis. Exogenously added SOD effectively induced neutrophil apoptosis, and the fluorescence patterns determined using annexin-V and the 7-AAD were similar to those seen in Fas-mediated neutrophil apoptosis. Neutrophils are short-lived leukocytes that need to be removed safely by apoptosis. The clearance of apoptotic neutrophils from sites of inflammation is a crucial determinant of the resolution of inflammation. Catalase inhibited the neutrophil apoptosis and caspase-3 activation. Spontaneous apoptosis, hydrogen peroxide and anti-Fas antibody-induced apoptosis of neutrophils were accelerated in Down's syndrome patients, in whom the SOD gene is overexpressed. Hydrogen peroxide was thought to be a possible major mediator of ROS-induced neutrophil apoptosis in caspase-dependent manner. Neutrophil apoptosis represents a crucial step in the mechanism governing the resolution of inflammation and has been suggested as a possible target for the control of neutrophil-mediated tissue injury. SOD may be a potential inhibitory mediator of neutrophil-mediated inflammation.

Adult↗
PubMed1996

Rat blood neutrophils express very late antigen 4 and it mediates migration to arthritic joint and dermal inflammation.

Blood neutrophils contribute to joint injury in human and experimental models of arthritis. Neutrophil migration out of the blood in joint inflammation involves both the CD18 (beta2) integrins and a CD18 integrin-independent pathway. To investigate this migration, radiolabeled rat blood neutrophils were used to measure neutrophil accumulation in the inflamed joints of rats with adjuvant arthritis and the role of leukocyte integrins in migration to these joints and to dermal inflammation was determined. Neutrophils migrated rapidly (<2 h) to the inflamed joints 14-18 d after immunization with adjuvant. Blocking monoclonal antibodies (mAbs) to both LFA-1 and Mac-1 together, as well as a mAb to CD18, inhibited neutrophil accumulation in the inflamed joints by 50-75%. However, migration to dermal inflammation induced by C5a(des Arg)' tumor necrosis factor alpha, lipopolysaccharide, and poly-inosine:cytosine was inhibited by approximately 90%. Flow cytometry revealed the expression of low levels of very late antigen 4 (VLA-4) on nearly all rat blood neutrophils. Treatment with anti-VLA-4 plus anti-LFA-1 but neither mAb alone, strongly (60-75%) inhibited neutrophil accumulation in arthritic joints. This mAb combination also inhibited neutrophil migration to dermal inflammatory reactions by 30-70%. Blocking VLA-4 together with the CD18 integrins inhibited neutrophil accumulation by 95-99%, virtually abolishing neutrophil accumulation in cutaneous inflammation. A similar blockade of VLA-4 and CD18 decreased neutrophil accumulation in the inflamed joints by 70-83%, but a significant portion of the neutrophil accumulation to these joints still remained. In conclusion, rat blood neutrophils express functional VLA-4 that can mediate neutrophil migration to both inflamed joints and dermal inflammatory sites. VLA-4 appears to be able to substitute for LFA-1 in this migration and is particularly important for accumulation in inflamed joints. However, there exists an additional CD18- and VLA-4-independent pathway of neutrophil migration to arthritic joints that is not involved in acute dermal inflammation.

Animals↗