Bleomycin-Induced Lung Injury/Pulmonary Fibrosis
Bleomycin is a chemotherapeutic agent used to treat cancers such as Hodgkins lymphoma. One of the side effects is pulmonary toxicity, which can be life threatening in approximately 10% of patients.
Murine Models of Allergic Asthma: OVA & HDM
Allergic Asthma is a complex, chronic inflammatory condition of the respiratory tract affecting approximately 300 million people worldwide, and is characterized by increased airway inflammation, airway hyper-reactivity, reversible airway obstruction and subsequent airway tissue remodeling.
Non-alcoholic steatohepatitis (NASH)
Non-alcoholic fatty liver disease (NAFLD) is a chronic condition affecting more than 30% of adults in the Western world that is characterized by accumulation of excess fat in the liver (hepatic steatosis) of people who drink little to no alcohol. While typically not considered a serious condition, NAFLD can develop into non-alcoholic steatohepatitis (NASH), which is a fatty liver accompanied byinflammation and various degrees of fibrosis that may develop into cirrhosis or HCC.
- MLM_Medical_Labs_Datasheet_NASH.pdf (668.16 KB)
DSS-induced Inflammatory Bowel Disease
The DSS model is a chemically-induced model of Inflammatory Bowel Disease (IBD) using dextran sodium sulphate (DSS) in the drinking water to induce ulcerative colitis-like inflammation. Acute colitis is induced by continuous administration of DSS over the course of 5 days.
Lipopolysaccharide (LPS) Acute Lung Inflammation Screen
Inflammation in pulmonary tissue is a complex interplay of multiple cellular and physiological responses to external stimuli and is commonly attributed to bacterial infection. Respiratory infec-tion can be mimicked via intranasal administration of lipopolysaccharide (LPS), providing a simple, rapid way to study acute host pulmonary inflam-matory response to bacterial exposure in the lungs.
Lipopolysaccharide (LPS) Lung Injury 24 and 72 hours
Lung inflammation induced by oral aspiration of LPS. Post euthanasia, lungs were inflated and fixed with formalin 10% for histological analysis.
Lipopolysaccharide (LPS) - induced Septic Shock
Sepsis is primarily defined as an intricate, systemic immune response to infection that can have seri-ous consequences, including multiple organ failure and death. The development and progression of sepsis is multi-factorial, and affects the cardiovas-cular, immunological and endocrine systems of the body. The complexity of sepsis makes the clinical study of sepsis and sepsis therapeutics difficult.
Mouse TNBS-induced Inflammatory Bowel Disease
TNBS-induced intestinal inflammation is com-monly used in mice as a model for IBD, particularly in reference to Crohns disease (CD). In this 7 day TNBS model, disease is induced through intrarectal administration of TNBS to produce clinically ame-nable indicators to that of CD such as diarrhea, rectal bleeding, body weight loss, more diffuse in-testinal inflammation, occasional adhesions, fibro-sis and vascularized ulceration.
Rat IMQ-induced Psoriasis
Psoriasis is the most common chronic autoim-mune skin condition, impacting ~125 million people worldwide. The pathogenesis of psoriasis is not wholly understood, though assumed to be a complex interplay between environmental factors, immune dysregulation and genetic susceptibil-ity. The imiquimod (IMQ) induced psoriasis model uses imiquimod, a TLR7 agonist, to activate innate immune cells in the skin. Diseased animals exhibit erythema and plaque formation shortly after the study begins and progresses through termination.
- MLM_Medical_Labs_Datasheet_IMQ_Rat_Psoriasis.pdf (129.23 KB)
Mouse IMQ-induced Psoriasis
Psoriasis is a very common skin disorder char-acterized by focal formation of inflamed, raised plaques that shed scales from excessive growth of epithelial cells and involves hyperplasia of epider-mal keratinocytes, vascular hyperplasia and extasia and infiltration of T lymphocytes, neutrophils and other types of leukocytes to affected skin.
As experts in skin inflammation modeling, MLM Medical Labs is proud to present its extensive ex-perience as one of the first laboratories to have validated the imiquimod induced psoriasis model in mice.
Systemic Sclerosis (SSc) is an autoimmune disease characterized by vasculopathy, fibrosis of the skin and internal organs, inflammation and general im-mune system abnormalities. MLM Medical Labs is using the chemotherapeutic antibiotic bleomycin, to induce SSc in CD-1 mice as a model to explore the pathogenic mechanisms involved in SSc. Imple-menting the use of osmotic minipumps containing bleomycin allows for a more stable and convenient SSc murine model that encompasses multiple fea-tures of human disease. This model may be used in therapeutic programs related to SSc, and more broadly, fibrotic diseases.
Peripheral Blood Mononuclear Cell (PBMC) Assays
Peripheral Blood Mononuclear Cells (PBMCs) are peripheral leukocytes isolated from whole blood which include T Cells, B Cells, NK Cells and Mono-cytes. PBMCs are a highly valuble research tool, providing an excellent cellular model for a wide range of applications and assessments of thera-pies that may act on inflammatory/immunological pathways (directly or indirectly).
- MLM_Medical_Labs_Datasheet_PBMC_Assays.pdf (138.84 KB)
Rat IL-23-induced Skin Inflammation
Skin inflammation affects millions of people each year. Recently, the IL-23/Th17 pathway has been shown to play a major role in skin inflammation pathogenesis making further mechanistic research a necessity. The IL-23-induced inflammation model is an ideal system with which to study this interplay.
Rat TNBS-induced Inflammatory Bowel Disease
TNBS-induced intestinal inflammation is com-monly used in rats as a model for IBD, particularly in reference to Crohns disease (CD). In this 7 day TNBS model, disease is induced through intrarectal administration of TNBS to produce clinically ame-nable indicators to that of CD such as diarrhea, rectal bleeding, body weight loss, more diffuse in-testinal inflammation, occasional adhesions, fibro-sis and vascularized ulceration. The TNBS model of IBD is pathologically driven by Th1/Th17 depen-dant mechanisms.