Calprotectin ELISA

Does Human Milk Fortifier Affect Intestinal Inflammation in Preterm Infants?

Eagle Biosciences’ Calprotectin ELISA Assay Kit was used in a recent study dealing with inflammation of preterm infants in response to human milk fortifier. The Calprotectin ELISA Assay is part of our line of Gastrointestinal Assays which is a line of highly sensitive and specific kits used to detect the concentration of a variety of samples in serum, plasma, tissue, urine, and saliva.


Background: Fecal calprotectin, a recognized marker of intestinal inflammation, is derived from neutrophil migration to a site of inflammation. Introduction of bovine-based human milk fortifier containing intact protein in preterm infants is associated with an increase in fecal calprotectin suggestive of intestinal inflammation. Newer fortifiers contain protein hydrolysates in place of intact protein.

Objective: To measure fecal calprotectin in human milk-fed preterm infants before and after human milk fortification using a fortifier containing hydrolyzed protein.

Methods: Serial stool samples were collected from 24 infants beginning at the first week to 60 days postnatal age. To compare the effect of human milk fortification, samples collected before and after fortification were compared. Infant demographics, diet, postnatal morbidities, and maternal characteristics were recorded.

Results: A total of 401 stool samples were collected from 24 study infants who had a birth weight of 993 ± 277 g (mean ± standard deviation), gestational age 27.5 ± 2.8 weeks, and fortifier initiation at 14 days. Median fecal calprotectin before and after fortification were similar. Calprotectin levels were not correlated with birth weight or gestational age but were inversely correlated with postnatal age (p = 0.005), use of fortifier (p < 0.001), receipt of antibiotics antenatally (p = 0.007) and postnatally (p = 0.008). After adjusting for postnatal age, calprotectin levels were significantly lower following receipt of fortifier (p < 0.001) and postnatal antibiotics (p < 0.001).

Conclusions: The feeding of protein hydrolysate-containing human milk fortifiers does not appear to be associated with increases in a marker of intestinal inflammation.

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Eagle Bioscience’s Calprotectin ELISA Assay Kit was recently used in a study dealing with bone loss in relation to arthritis and other inflammatory diseases. The Calprotectin ELISA Assay is part of our line of Gastrointestinal Assays which is a line of highly sensitive and specific kits used to detect the concentration of a variety of samples in serum, plasma, tissue, urine, and saliva.

Blood-induced bone loss in murine hemophilic arthropathy is prevented by blocking the iRhom2/ADAM17/TNFα pathway


Hemophilic arthropathy (HA) is a debilitating degenerative joint disease that is a major manifestation of the bleeding disorder Hemophilia A. HA typically begins with hemophilic synovitis (HS) that resembles inflammatory arthritides such as rheumatoid arthritis (RA) and frequently results in bone loss in patients. A major cause of RA is inappropriate release of the pro-inflammatory cytokine tumor necrosis factor α (TNFα) by the TNFα convertase (TACE, also referred to as ADAM17) and its regulator, iRhom2. Therefore, we hypothesized that iRhom2/ADAM17-dependent shedding of TNFα also has a pivotal role in mediating HA. Here, we show that addition of blood or its components to macrophages activates iRhom2/ADAM17-dependent TNFα shedding, providing the premise to study the activation of this pathway by blood in the joint in vivo. For this, we turned to hemophilic FVIII-deficient mice (F8-/- mice), which develop a hemarthrosis following needle puncture injury with synovial inflammation and significant osteopenia adjacent to the affected joint. We found that needle puncture-induced bleeding leads to increased TNFα levels in the affected joint of F8-/- mice. Moreover, inactivation of TNFα or iRhom2 in F8-/- mice reduced the osteopenia and synovial inflammation that develops in this mouse model for HA. Taken together, our results suggest that blood entering the joint activates the iRhom2/ADAM17/TNFα pathway, thereby contributing to osteopenia and synovitis in mice. Therefore, this pro-inflammatory signaling pathway could emerge as an attractive new target to prevent osteoporosis and joint damage in HA patients.

Haxaire, Coline, et al. “Blood-Induced Bone Loss in Murine Hemophilic Arthropathy Is Prevented by Blocking the iRhom2/ADAM17/TNFα Pathway.” Blood, 18 May 2018, 

EagleBio’s Calprotectin ELISA was recently used in a study done by the University of North Carolina. This assay is a part of our Gastrointestinal Assay Kit line which is comprised of a unique set of products that can be used in a variety of applications, research, and fields of study. Check out the product page for full details on this kit, or click the link below to view the new publication referencing out Calprotectin ELISA Assay.

Becker-Dreps, Sylvia,
Samuel Vilchez, Filemon Bucardo, Erica Twitchell, Wan Suk Choi, Michael G.
Hudgens, Johann Perez, and Lijuan Yuan. “The Association Between Fecal
Biomarkers of Environmental Enteropathy and Rotavirus Vaccine Response in
Nicaraguan Infants.” The Pediatric Infectious Disease Journal36.4
(2017): 412-16. Web.…

“Environmental enteropathy (EE) is a common intestinal condition among children living in low- and middle-income countries and is associated with diminished enteric immunity to gastrointestinal pathogens, and possibly to oral vaccine antigens. The goal of this study was to examine associations between biomarkers of EE and immunogenicity to the pentavalent rotavirus vaccine (RV5).” Read More.