Rat INF-α-Ab(Interferon-α Antibody) ELISA Kit

Name: Rat INF-α-Ab(Interferon-α Antibody) ELISA Kit
SKU: DEIA-BJ2164
Rating: 5 (1 reviews)

Regulatory status: For research use only, not for use in diagnostic procedures.

COA

SDS

Datasheet

Summary

Sample

Serum, plasma, other biological fluids

Species Reactivity

Rat

Detection Method

sELISA

Intended Use

INF-α-Ab ELISA Kit allows for the in vitro quantitative determination of INF-α-Ab concentrations in serum, plasma, tissue homogenates and other biological fluids.

Contents of Kit

Storage

2-8°C for 6 months

Precision

Intra-Assay: CV<8%
Inter-Assay: CV<10%

Detection Range

1.563-100ng/ml

Sensitivity

0.938ng/ml

Standard Curve

Results of a typical standard operation of a INF-α-Ab ELISA Kit are listed below. This standard curve was generated at our lab for demonstration purpose only. Users shall obtain standard curve as per experiment by themselves. (N/A=not applicable)

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Differential activities of alpha/beta IFN subtypes against influenza virus in vivo and enhancement of specific immune responses in DNA vaccinated mice expressing haemagglutinin and nucleoprotein

VACCINE

Authors: James, Cassandra M.; Abdad, Mohammad Y.; Mansfield, Josephine P.; Jacobsen, Hege K.; Vind, Azita Rezazadeh; Stumbles, Philip A.; Bartlett, Emmalene J.

Abstract

Vaccines are urgently needed to elicit immunity to different influenza virus strains. DNA vaccines can elicit partial protective immunity, however their efficacy requires improvement. We assessed the capacity of individual type I IFN multigene family members as subtype transgenes to abrogate influenza virus replication in a vaccination/challenge mouse model. Differences in antiviral efficacy were found among the subtypes with IFNA5 and IFNA6 being most effective, while IFNA1 was the least effective in reducing lung virus replication. Mice vaccinated with combinatorial HA/IFNA6 or NP/IFNA6 showed reduced lung viral titres, clinical score, body weight loss, and pulmonary tissue damage compared to IFNA6, HA, or NP viral vaccination alone. In addition, IFNA6 increased IaG2a titres with upregulation of IFNgamma response in the respiratory tract. We conclude that IFN-alpha 6 has antiviral and immunomodulatory effects, which improve efficacy of DNA vaccines for enhanced control of influenza. (c) 2006 Elsevier Ltd. All rights reserved.

Glibenclamide alters interleukin-8 and interleukin-1 beta of primary human monocytes from diabetes patients against Mycobacterium tuberculosis infection

TUBERCULOSIS

Authors: Kewcharoenwong, Chidchamai; Saenwongsa, Wipawee; Willcocks, Samuel J.; Bancroft, Gregory J.; Fletcher, Helen A.; Lertmemongkolchai, Ganjana

Abstract

Type 2 diabetes mellitus (T2DM) is an important risk factor for development of tuberculosis (TB). Our previous study showed glibenclamide, an anti-diabetic drug used to control blood glucose concentration, reduced interleukin (IL)-8 secretion from primary human monocytes challenged with M. tuberculosis (Mtb). In mice infected with Mtb, IL-1 beta is essential for host resistance through the enhancement of cyclooxygenase that limits excessive Type I interferon (IFN) production and fosters Mtb containment. We hypothesize that glibenclamide may also interfere with monocyte mediated immune responses against Mtb and alter the balance between IL-1 beta and IFN alpha-mediated immunity. Purified monocytes from non-diabetic and diabetic individuals were infected with Mtb or M. bovis BCG. We demonstrate that monocytes from diabetes patients who were being treated with glibenclamide showed reduced IL-1 beta and IL-8 secretion when exposed to Mtb. Additionally, these responses also occurred when monocytes from non-diabetic individuals were pre-treated with glibenclamide in vitro. Moreover, this pre-treatment enhanced IFNa1 expression but was not involved with prostaglandin E2 (PGE2) expression in response to Mtb infection. Taken together, our data show that glibenclamide might exacerbate susceptibility of diabetes patients to Mtb infection by reducing IL-1 beta and IL-8 production by monocytes.