Lung inflammatory responses

Inflammation is an important manifestation of respiratory disease in domestic animals. The respiratory system is mucosal in nature and has specific defense mechanisms used to control invasion by microbes and environmental elements. Inflammation can be beneficial or detrimental to the host. This article broadly discusses the primary mediators and mechanisms of inflammation within the respiratory tract of domestic animals. The role of cells, chemokines, cytokines and mediators in both acute and chronic inflammation are addressed. The pathogenesis of the initial insult determines the type of inflammation that will be induced, whether it is acute, chronic or allergic in origin. Maintenance of the microenvironment of cytokines and chemokines is critical for pulmonary homeostasis. Uncontrolled inflammation in the respiratory tract can be life threatening to the animal. The understanding of the mechanisms of inflammation, whether due to microbes or through inappropriate immune activation such as those occurring with allergies, is required to develop successful intervention strategies and control respiratory disease in animals.     

Management of intraocular inflammatory disease

The uvea of the eye is divided into the anterior uvea (iris and ciliary body) and posterior uvea (choroid). Clinical signs of anterior uveitis include conjunctival hyperemia, corneal edema, aqueous flare, miosis, and a decrease in intraocular pressure. Inflammation of the posterior uvea often involves the retina as well resulting in a chorioretinitis. Clinical signs of chorioretinitis may include multifocal lesions in tapetal or nontapetal fundus, retinal detachment, and a decrease in vision. The etiology of uveitis is complex and includes numerous infectious, neoplastic, immune-mediated, and other diseases. Treatment is directed at the underlying systemic disease, if present, as well as symptomatic treatment for the eye. The diagnostic and therapeutic approach to a patient with uveitis is discussed.     

Canine chronic inflammatory rhinitis

Chronic inflammatory rhinitis is commonly found in dogs with chronic nasal disease and is characterized by lymphoplasmacytic infiltrates in the nasal mucosa in the absence of an obvious etiologic process. The pathogenesis of lymphoplasmacytic rhinitis remains unknown. Animals respond poorly to antibiotics, oral glucocorticoids, and antihistamines, making primary infectious, immune-mediated, or allergic etiologies unlikely. Aberrant immune response to inhaled organisms or allergens may induce inflammation in some animals. Common clinical signs include nasal discharge, sneezing, coughing, epistaxis, and stertor. Diagnosis is made by performing a thorough history, physical examination, radiography or advanced imaging (via computed tomography or magnetic resonance imaging), rhinoscopy, and nasal mucosal biopsy to rule out primary etiologies of nasal discharge. Treatment strategies have included various antibiotics, antihistamines, oral and inhalant steroids, nonsteroidal antiinflammatories, and antifungal medications. Some dogs may respond partially to doxycycline or azithromycin, although it is unclear whether response is related to antimicrobial or antiinflammatory properties of these drugs. Hydration of the nasal cavity through nasal drops or aerosols may limit nasal discharge, and some animals may improve with inhalant (but rarely oral) glucocorticoids.     

Apoptosis of resident and inflammatory macrophages before and during the inflammatory response of the virgin bovine mammary gland

Background

Macrophages may play a prominent role in defense of the bovine mammary gland, and their functionality is necessary for successful eradication of bacterial pathogens. In contrast to necrosis, however, apoptosis has not yet been studied in macrophages from bovine mammary glands. Therefore, the aim of this study was to confirm the occurrence of apoptosis in macrophages from resting heifer mammary glands and during the inflammatory response.

Methods

Inflammatory response was induced by phosphate buffered saline (PBS) and by lipopolysaccharide (LPS). Resident macrophages (_RESMAC) were obtained before and inflammatory macrophages (_INFMAC) 24, 48, 72 and 168 hours after inducing inflammatory response in mammary glands of unbred heifers. Cell samples were analyzed for differential counts, apoptosis and necrosis using flow cytometry.

Results

Populations of _RESMAC and _INFMAC contained monocyte-like cells and vacuolized cells. Apoptosis was detected differentially in both morphologically different types of _RESMAC and _INFMAC and also during initiation and resolution of the inflammatory response. In the _RESMAC population, approximately one-tenth of monocyte-like cells and one-third of vacuolized cells were apoptotic. In the _INFMAC population obtained 24 h after PBS treatment, approximately one-tenth of monocyte-like cells and almost one-quarter of vacuolized cells were apoptotic. At the same time following LPS, however, we observed a significantly lower percentage of apoptotic cells in the population of monocyte-like _INFMAC and vacuolized _INFMAC. Moreover, a higher percentage of apoptotic cells in _INFMAC was detected during all time points after PBS in contrast to LPS. Comparing _RESMAC and _INFMAC, we observed that vacuolized cells from populations of _RESMAC and _INFMAC underwent apoptosis more intensively than did monocyte-like cells.

Conclusions

We conclude that apoptosis of virgin mammary gland macrophages is involved in regulating their lifespan, and it is involved in the resolution process of the inflammatory response.     

Management of inflammatory polyps in 37 cats

The case records of 37 cats treated for nasopharyngeal or aural inflammatory polyps were reviewed. Thirty of them were managed conservatively with the polyp being removed by traction alone. Long-term follow-up information was available for 22 cats, of which 13 (59 per cent) had no recurrence of clinical signs. The remaining nine cats required recurrent polyps to be removed surgically. Cats with only nasopharyngeal polyps were nearly four times more likely to be cured by traction alone than cats with aural polyps, and none of the cats that was treated with prednisolone after traction suffered a recurrence. Cats with more severe aural signs were more likely to require surgery.     

Practical cytology for inflammatory skin diseases

Cytology is the most common and immediately informative diagnostic tool in the practice of dermatology. It is simple to perform and requires equipment usually already present in most practices such as a microscope and slides, cotton-tipped applicators and stains. Cytology interpretation is also easily self taught. With little practice the practitioner can easily become familiar with sample interpretation from inflammatory lesions; including recognition of bacteria, yeast, dermatophyte spores and hyphae, deeper fungal elements and parasites. Additionally, the practitioner should become familiar with the variety of inflammatory cells seen with these conditions, as well as keratinocyte morphology. This article provides an overview and the initial steps on how to become a more proficient cytologist in practice.     

Bartonella-associated inflammatory cardiomyopathy in a dog

A 6-year-old, male, mongrel dog was presented for acute onset of dyspnea and cough. At admission, the dog was cachectic and severely depressed. The electrocardiogram showed a sinus rhythm conducted with left bundle truncular branch block and interrupted by frequent multiform ventricular ectopic beats organized in allorhythmias. Thoracic radiographs revealed a marked cardiomegaly with perihilar edema, whereas transthoracic echocardiography revealed a dilated cardiomyopathy with segmental dyskinesis. Furosemide, enalapril, pimobendan, and mexiletine were prescribed, and a Holter was scheduled after resolution of congestive heart failure. Three days later, the dog died suddenly during sleep. Histopathology revealed diffuse myocyte hypertrophy with multifocal hemorrhages, alternating to areas of severe replacement fibrosis and lymphoplasmocytic infiltrates. Immunohystochemistry stains were strongly positive for T-lymphocyte infiltration (CD3) and weakly positive for B-lymphocytes (CD79). Polymerase chain reaction was positive for Bartonella spp. Based on these results, a post-mortem diagnosis of bacterial inflammatory cardiomyopathy was made.     

Immunology of inflammatory diseases of the bowel.

During the past century, research on animal diseases has focused on the characterization of specific etiologies and disease control strategies. Many diseases affecting domestic animals have been successfully controlled using various methods, including vaccination, management, vector control, or antimicrobial agents. A number of microorganisms have proven resistant to these efforts. Control of these organisms requires the development of new strategies. As practitioners and researchers, we need to consider approaches that encompass the entire realm of disease expression from molecular to immune responses and interactions with other functional systems (e.g., endocrine, neurologic, and vascular systems). We need a basic understanding of effective immune responses enabling the tailoring of vaccines to produce the desired response. This tailoring of host responses is augmented by the use of vaccines that use host growth factors, cytokines, or costimulatory molecules to bias the ensuing response. Intestinal microbial flora of food-producing animals can be managed to optimize health and minimize colonization by pathogenic organisms, especially zoonotic agents. New systems for the delivery of cytokines and other factors that favor optimal intestinal health and homeostasis need to be researched and evaluated. With time, it is likely that our clients and the consumers will be less tolerant of antibiotic usage. They will be more aware of the zoonotic potential of many microbes that colonize food animals. Food safety issues will be a continuing concern, as will the protection of our water supply from contamination from feedlots and pasture runoff. We are in the dawn of a new century, and, it is hoped, a new era of discovery of enteric disease pathogenesis and control.     

Carrageenan-induced acute inflammatory response in chicks

Carrageenan from two commercial sources was used in varying concentrations to evoke an acute inflammatory response in the foot pad of chickens. Oedema formation and increased vascular permeability were less severe using this experimental model than with turpentine-induced injury. Inflammation was monophasic, of short duration and apparently mediated by histamine and serotonin as their respective antagonists diminished the response. Prostaglandins seemed to play only a minor role as indomethacin blocked only the later phase of oedema. Bothrops jararaca venom did not potentiate the inflammatory response, implying that bradykinin was not a significant mediator.     

Chronic idiopathic inflammatory bowel diseases of the horse

A review of reported cases of inflammatory bowel diseases (IBDs) of horses for which no etiology was identified included cases of granulomatous enteritis (GE), multisystemic eosinophilic epitheliotropic disease (MEED), lymphocytic-plasmacytic enterocolitis (LPE), and idiopathic eosinophilic enterocolitis (EC). The terms EC and MEED were both used to describe a disease in horses characterized by infiltration of intestine and extraintestinal tissues with eosinophils. We use EC to describe IBD characterized by only intestinal infiltration by eosinophils. Horses with GE, MEED, or LPE are usually examined because of weight loss and depression, but horses with EC are usually examined because of signs of abdominal pain. Typically, horses with IBD have low concentrations of serumal proteins, especially albumin, and fail to adequately absorb glucose or xylose. Antemortem diagnosis of IBD can only be made by histologic examination of affected intestine. In some cases, antemortem diagnosis is made from histologic examination of rectal mucosa obtained by biopsy. Suspected causes of IBD in the horse include abnormal immune response to bacterial, viral, parasitic, or dietary antigens. Most horses with IBD do not survive, but horses with EC are more likely than those with LPE, MEED, or GE to respond to treatment. Successful treatments of horses with IBD include resection of grossly affected intestine and administration of corticosteroids.     

Late-stage mediators of the inflammatory response: identification of interleukin-1 and a casein-degrading enzyme in equine acute inflammatory exudates

Interleukin-1 and a casein-degrading enzyme have been identified in an experimental system for studying acute inflammation in the horse. The levels of both the cytokine and the proteinase increased over the first 24 hours following initiation of the inflammatory response, and remained at high levels through to the last sample collected at 48 hours. This is in marked contrast to prostaglandin E2 concentrations which were low initially, peaked at four to eight hours and had returned to low levels by 12 to 24 hours. It is likely that interleukin-1 and various proteinases are involved in the later stages of the inflammatory response, such as the tissue remodelling associated with wound repair, and control of this cytokine may be important in the progression from acute to chronic inflammation.     

Matrix metalloproteinases in inflammatory pathologies of the horse

The extracellular matrix (ECM) of connective tissue is constantly being remodelled to allow for growth and regeneration. Normal tissue maintenance requires the ECM components to be degraded and re-synthesised in relatively equal proportions. This degradation is facilitated by matrix metalloproteinases (MMPs) and their proteolytic action is controlled primarily by the tissue inhibitors of metalloproteinases (TIMPs). Both MMPs and TIMPs exist in a state of dynamic equilibrium, with a slight excess of one or the other depending on the need for either ECM breakdown or synthesis. Long-term disruption to this balance between MMPs and TIMPs will have pathological consequences.Matrix metalloproteinases are involved in a number of diseases in mammals, including the horse. Excess MMP activity can cause ECM destruction, as seen in the lamellar basement membrane in laminitis and the articular cartilage in osteoarthritis. Matrix metalloproteinase under-activity can potentially impede healing by preventing fibrinolysis in fibrotic conditions and the removal of scar tissue in wounds. Matrix metalloproteinases also degrade non-ECM proteins and regulate cell behaviour via the release of growth factors from the substrates they cleave, increasing the scope of their effects. This review looks at the involvement of MMPs in equine health and pathologies, whilst exploring the potential consequences of therapeutic intervention.