Neutrophil-to-lymphocyte ratio may predict renal function decline in diabetes

Researchers have found that Neutrophil-to-lymphocyte ratio is a predictor of renal dysfunction in diabetes patients.The study has been published in Diabetes Metabolic Syndrome: Clinical Research & Reviews. 

Inflammation play an important role in the pathogenesis of diabetic kidney disease.Neutrophil-to-lymphocyte ratio has been evaluated as a biomarker of inflammation and has been widely evaluated as a biomarker in various medical and surgical prognoses.However its usefulness in diabetic kidney disease is not yet known.

The researchers conducted a prospective observational study that included outpatients, comprising of 184 men aged 73 ± 11 (mean ± standard deviation) years and 174 women aged 76 ± 10 years at baseline, from a rural hospital. They examined the relationship between baseline NLR calculated by analyzing the differential leukocyte counts in the complete blood count and the 2-year estimated glomerular filtration rate (eGFR) decline rate (i.e. 2-year eGFR-baseline eGFR) ∗100/baseline eGFR. Rapid eGFR decline rate was defined as a value < -25%.

The researchers found that NLR (β = 0.138, p = 0.007) as well as presence of antidyslipidemic medication, hemoglobinA1c, and urinary albumin excretion stage were significantly and independently associated with a rapid eGFR decline rate.The multiple linear regression analysis using rapid eGFR decline rates as objective variables were adjusted for confounding factors as explanatory variables. 

The multivariate-adjusted odds ratios (95% confidence interval) of the 2nd and 3rd tertiles of baseline NLR for rapid eGFR decline rate were 3.62 (0.70-18.7) and 8.03 (1.54-41.9), respectively. 

Multivariate-adjusted mean eGFR (95% confidence interval) values after 2 years categorized by tertile of baseline NLR were: 1st, 63.9 (61.8-66.1); 2nd, 60.8 (58.7-62.9); and 3rd, 58.9 (56.8-61.0).
The researchers concluded that these results suggest that baseline Neutrophil-to-lymphocyte ratio might be a useful biomarker for renal function decline in outpatients with type 2 diabetes. This biomarker may help evaluate renal function in diabetics.

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Antibody-based eye drop may treat dry eye disease

Researchers at the University of Illinois at Chicago are the first to identify the presence of a specific type of antibody, called anti-citrullinated protein autoantibodies, or ACPAs, in human tear fluid. They are also the first to demonstrate that patients with dry eye disease experienced reduced signs and symptoms of the condition in response to a new eye drop treatment —- made from pooled human antibodies—that targets ACPAs. 

The findings from their early stage clinical trial are reported in the journal.

Dry eye disease is caused by abnormalities in the tear fluid and results in dry areas over the cornea, the transparent outer layer of the eye, which can lead to disabling eye pain and sensitivity to light in severe cases.

"The burden of autoimmune dry eye is much greater than just having an occasional feeling of dryness," said the senior author of the study. "It can severely compromise quality of life to the point of disability and can compromise a person's vision."

In previous research, researchers discovered that strands of DNA extrude from neutrophils, a type of white blood cell, to form webs on the surface of eyes affected by severe dry eye disease and cause inflammation.

In the new study, the researchers identified ACPAs as another cause of eye inflammation that also contributes to the development of these webs, which Jain calls "a vicious cycle of inflammation."
The new eye drops treat dry eye disease by knocking the immune system out of this cycle, at least partially.

The drops are formulated using pooled antibodies—which are made from immune globulins processed from the donated blood of thousands of individuals, all containing varied types of antibodies—that counteract the negative effects of ACPAs.

The phase I/II drug trial compared the antibody-based eye drops with eye drops without the antibodies.

"There are currently only two approved drugs to treat dry eye, and they don't work for everyone, especially those with severe disease, so having a new drug that can treat the disease by targeting a different mechanism, in this case, an autoimmunity, is very important," the Dr. said.

Twenty-seven participants with severe dry eye disease participated in the trial. The participants were randomized into two groups. One group was given eye drops made from pooled antibodies and instructed to administer one drop to each eye twice daily for eight weeks. The control group was given the same instructions with eye drops made without antibodies.

The researchers evaluated patients' symptoms through questionnaires and measured the extent of corneal damage and the amount of pro-inflammatory biomarkers on the surface of the eye before and for the duration of the study.

They found that people using antibody-based eye drops had a statistically significant and clinically meaningful reduction in corneal damage at eight weeks compared with the control group. 

Questionnaire scores related to symptoms also reflected significant improvement among patients using the new antibody-based eye drops when compared with the eye drops without antibodies. In the test group, the amount of pro-inflammatory biomarkers—or dry areas—also was reduced on the surface of the eye.

"Participants in the trial who used the drops with pooled antibodies reported less eye discomfort and their corneas were healthier," Jain said. "The data from this early clinical trial suggests that eye drops containing pooled antibodies may be safe and effective for treating dry eye disease, and we look forward to conducting larger randomized trials to definitively prove its efficacy."

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‘Secret handshake’ detected between sperm and uterus

A team of researchers has discovered the making of a “secret handshake” between sperm and the cells lining the uterus that finally let one sperm out of nearly 200 million to make it through and fertilise a single egg, say researchers.

Uterine cells express a receptor that recognizes a glycan molecule on the surface of sperm cells.

It’s possible that this interaction may adjust the female’s immune response and help sperm make it through the leukocytic reaction, said the researchers. The leukocytic reaction is not well understood.

What we do know, explained molecular anthropologist  is that “after crossing the cervix, millions of sperm that arrive in the uterus are faced by a barrage of macrophages and neutrophils”.

This attack by the innate immune system kills a majority of the sperm cells in semen, winnowing hundreds of millions of sperm down to just a few hundred that enter the fallopian tubes.

The defensive response may be beneficial in preventing polyspermy, when an egg is fertilized by more than one sperm and cannot develop.

“It’s somewhat embarrassing how little we can say about what this [interaction] means,” said  a researcher.

Reproduction, he said, “is a very, very delicate tug-of-war at many levels. The fact that there is (also) this immune game going on is completely fascinating.”

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IIT Kanpur identifies novel molecule to control hyper inflammation

Researchers at the Indian Institute of Technology (IIT) Kanpur have identified and characterised a novel small protein molecule that can effectively control inflammation leading to better treatment outcomes. In contrast, inflammation control by molecules that are undergoing clinical trials may not be optimal due to inherent drawbacks. The work was done in collaboration with the University of Queensland.

Hyper inflammation

While some amount of inflammation at the site of infection is required for effective clearance of pathogens, too much inflammation compromises pathogen-clearing ability. Hyper inflammation also destroys the tissues surrounding the inflamed area leading to inflammation disorders such as sepsis, inflammatory bowel syndrome, rheumatoid arthritis and psoriasis. 

A small protein (C5a) that is a part of the innate immunity (immediate defence against pathogens that have never been encountered before) gets activated when a pathogen enters the body. The C5a protein then binds to a particular receptor (C5aR1) found on the surface of certain cells such as macrophages and neutrophils to begin the process of inflammation and pathogen clearance.

Neutrophiles are already present in the body and circulate in the blood. Once the small protein binds to the C5aR1 receptor found on neutrophils, there is increased migration towards the site of infection leading to hyper inflammation. At the same time, binding of the small protein to the receptor on macrophages reduces the amount of a pro-inflammatory cytokine called interleukin-6 (IL-6) that is released, which is desirable to overcome inflammatory symptoms. 

Therapeutic agents now undergoing clinical testing prevent the C5a protein from binding to the receptor found on neutrophils leading to reduced migration of neutrophils to the site of infection. Hyper inflammation is thus prevented. However, it has the opposite effect on interleukin-6 release. Unlike the C5a protein, the drug candidate molecules do not reduce the amount of IL-6 being released thereby causing more inflammation.

Role of IL-6

“There is more inflammation when the amount of IL-6 at the site of infection is more. So it is desirable to reduce the amount of IL-6 being released to overcome the inflammatory symptoms,” says a researcher.

The small protein molecule identified by IIT Kanpur researchers addresses the shortcomings seen with the drug molecules now undergoing clinical testing. The drug molecule that IIT Kanpur team used for this study is already known to bind to the C5aR1 receptor. But its effects were not characterised in term of IL-6 release and neutrophil migration.

“Our peptide molecule binds to the C5aR1 receptor found on neutrophils and reduces their migration to the site of infection. And unlike the molecules now being tested, our peptide molecule also reduces the amount of IL-6 being released,” says a Prof. Under in vitro conditions, the combined effect may lead to reduced inflammation.

“The molecule only reduces and not blocks neutrophil migration. There should be sufficient inflammation at the infection site to clear the pathogens,” says the first author of the paper.

The peptide molecule identified by the team is smaller than the C5a protein so the binding to the receptor is weak. “So we have to use higher concentration of our synthetic peptide to achieve better results. Future work would be to increase the strength of binding by improving the molecule so that less concentration is needed,” the Prof. says. The team plans to carry out animal studies in future to measure the therapeutic potential of the molecule.

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All About Your White Blood Cells

White blood cells (WBCs) form the part of your immune system which is responsible for fighting infection and defending the body against other foreign materials. Various kinds of WBCs are involved in recognizing intruders, destroying harmful bacteria, and synthesizing antibodies to defend your body from future exposure to nasty bacteria and viruses.

Types of White Blood Cells
There are 5 main types of white blood cells, which include:
Neutrophils - Around half of your white blood cells are neutrophils. These cells are normally the first to appear in response to threats. As first responders, they also send out messages which alert other immune cells to respond. Your body produces close to 100 billion neutrophils each day, and once they are released from the bone marrow live for only 8 hours.
Lymphocytes (B lymphocytes and T lymphocytes) - There are 2 types of lymphocytes, with T cells being responsible for directly killing infections, while B cells are responsible for humoral immunity. They create the antibodies which "remember" a threat and stand ready in case your body should ever be exposed to them again.

Monocytes - Monocytes are practically your immune system's garbage trucks. Around 5 percent of your white blood cells are monocytes, and their most essential function is to move into tissue and clean up any dead cells.
Eosinophils - Eosinophils play a critical role when it comes to fighting off bacteria, and they are also very important in responding to parasitic infections. They are also notorious for their role in producing allergy symptoms when they essentially believe that something harmless (such as pollen) is an invader. These are only around 1% of the white blood cells in your body but are highly concentrated in the digestive tract.

Basophils - Basophils also make up only 1% of your body's white blood cells, and are important in mounting a non-specific immune response to infections. Basophils are best known for their role in asthma, since their stimulation may result in the inflammation and bronchoconstriction of your airways.

Conditions Involving High White Blood Cell Levels

There are a number of reasons why a person's white blood cell count may be too high, including:

• Infections
• Stress
• Exercise
• Certain cancers
• Inflammation
• Autoimmune disorders
• Trauma ranging from emotional stress to fractures
• Pregnancy
• Asthma
• Allergies 

Conditions With Low White Blood Cell Levels

There are also quite a few reasons as to why white blood cell levels could be too low, including:

• Severe infections
• Bone marrow damage
• Aplastic anemia
• Drug or chemical-related damage to your bone marrow
• Autoimmune diseases such as lupus
• Splenic sequestration

Symptoms of a Low White Blood Count

A low white blood cell count may be accompanied by quite a number of symptoms. These may include:

• Blood in the stools
• Fever
• Cough
• Pain or frequency of urination
• Diarrhea
• Redness, swelling, or warmth in a region of infection

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Scientists identify new approaches to treat inflammatory arthritis

Researchers have identified a molecule required for immune cells to enter the joints that could lead to new treatment approaches for inflammatory arthritis. Researchers of the Massachusetts General Hospital (MGH) have found that that tracking immune cells can assist in identification of inflammatory arthritis. The findings indicate that specific molecule – complement C5a – is required to cause the immune cells called neutrophils to adhere to joint surfaces and migrate into the joint, a process known to set off the inflammatory cascade. The study, published in the journal of Science Immunology, has identified the initial steps leading to joint inflammation in a model of inflammatory arthritis. ‘Inflammatory arthritis is caused when immune cells are recruited from the blood into the joint in a highly regulated process controlled by chemoattractants and adhesion receptors,’ said senior author Andrew Luster. ‘But when the disease has become symptomatic, it is difficult to determine the initial steps that set off the recruitment of immune cells into the joint and the specific roles of the different chemoattractants,’ Luster added.

To better determine the role of specific chemoattractants in type III hypersensitivity, lead author Yoshishige Miyabe, used multiphoton intravital microscopy – an imaging technology for studying immune cell movements in living animals. The results revealed that the presence of ICs within the joint space induces the generation of complement C5a, a component of the innate immune system, which is then displayed on the inner walls of adjacent blood vessels. C5a directly initiates the adherence of neutrophils to the vessel walls through interaction with the C5a receptor on neutrophils, which then pass into the joint space and set off the inflammation. ‘The control of immune cell entry into the joint represents a major point at which new therapies could be developed to reduce the symptoms of inflammatory arthritis,’ Luster stated

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Newborns have strong immune system

Although their immune system works very differently from that of adults, babies may be able to mount a stronger immune defence than previously thought, a study suggests.

Contrary to what was previously thought, newborn immune T-cells may have the ability to trigger an inflammatory response to bacteria, the findings showed.

"We found that babies have an in-built anti-bacterial defence mechanism that works differently to adults, but nevertheless may be effective in protecting them," said lead author of the study Deena Gibbons from King's College London in Britain.

"This may also be a mechanism by which the baby protects itself in the womb from infections of the mother," Gibbons added.

Up to now, it was generally believed that babies have an immature immune system that does not trigger the same inflammatory response normally seen in adults.

Although babies need to protect themselves from the harmful pathogens they are exposed to from birth, it was thought that their T-cells were suppressed to some extent to prevent inflammatory damage to the developing child.

Skeptical of this notion, the researchers set out to characterise the properties of T-cells, examining very small samples of blood in 28 highly premature babies, as they developed over the first few weeks of their life.

While T-cells in newborn babies are largely different to those in adults, it is not because they are immuno-suppressed; rather, they manufacture a potent anti-bacterial molecule known as IL8 that activates neutrophils to attack the body's foreign invaders.

The study appeared in the journal Nature Medicine.

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