*Erythrocyte - A Peripheral Biomarker for Infection and Inflammation* is divided into two sections: "Cells with a Signature" and "Functional Biomarkers."

The first chapter in Section 1 describes the role of iron deficiency (ID) in erythrocytes in regulating anaemia and heart failure. In heart failure, the ID rather than anaemia serves as the predictor for clinical outcome. In fact, ID has been shown to be a stronger predictor of the patients outcome than anaemia. ID without anaemia carries greater risk and poorer outcome compared to an anaemic patient without ID.

The second chapter in Section 1 discusses the role of erythrocytes in immunology, their interaction with viruses, metal ions, trace elements, and reactive oxygen species, and their involvement in sepsis and genetic disorders. It also examines the modulation of oxidative stress (OS) in erythrocytes in bacterial and viral infections. This chapter demonstrates how variations in RBC's proteins, lipids, and antioxidant capacity can be used as an OS biomarker to evaluate the efficiency of the erythrocytes in response to oxidative insults due to viral or bacterial intrusion. These infections alter the antioxidant capacity of erythrocytes, causing damage to surrounding cells and tissues. Thus, OS biomarkers can be used to gain insights into the effects of bacterial and viral infections on the erythrocyte microenvironment which is described in the third chapter.

Section 2 begins with a chapter describing how to measure early predictive biomarkers for hypertension by using human foetal astrocytes (HFAs) as an experimental model. The authors explain and demonstrate why and how HFAs are a good model for the detection of biomolecules that can predict the future onset of high blood pressure. Long processes of HFAs are mainly supported by intermediate filaments (IF), and glial fibrillary acidic protein (GFAP) is classified as a type III intermediate filament protein that is abundantly present in astrocytes. Elevated GFAP levels are being considered as a marker of astroglial injury, indicating the conversion of non-reactive (A2) into reactive (A1) astrocytes.

In this study, the authors also demonstrate that astrocytes from spontaneous hypertensive rats (SHRs) and their normal counterparts (WKY) rats have a remarkably similar profile of GFAP intensity to that of reactive (A1) and non-reactive (A2) HFAs, indicating that the HFA model can be used to study hypertension. They observed that reactive (A1) HFAs contain more calcium-activated proteins such as calpain, calpastatin, cathepsin, and mitogen-activated protein kinase (MAPK) as compared to normal (A2) HFAs, suggesting the possible link of these proteins with the future onset of HTN. Hence these proteins could be considered as potential candidates for predictive biomarkers of HTN. Similarly, DNA damage by polycyclic aromatic hydrocarbons was detected in the white blood cells (WBCs) of asphalt plant workers and evaluated by measuring the Benzo[a]pyrene diol epoxide (BPDE)-DNA in their WBCs. In the fifth chapter, the authors clearly show the carcinogenic effects of B[a]P on the workers in the asphalt company and that these BPDE-DNA adducts can act as biological markers for exposure risk assessment. Finally, in the last chapter the readers will be interested to know that there is an exponential increase in the risk of arterial and venous thrombotic events with age, gender, smoking habits, and diet types. The authors demonstrate an association of arterial thrombosis with ABO blood group, age, gender, smoking habit, and Rh, Kell, and MN blood groups in a population in Georgia.

I hope readers will achieve a better understanding of the various aspects of erythrocytes and their interaction with other cells in the blood and other tissues.

I would like to thank Author Service Manager Mr. Josip Knapic for his hard work, constant support, and help.

> **Kaneez Fatima Shad** School of Life Sciences, UTS, Sydney, Australia

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Section 1

Cell with a Signature

Section 1 Cell with a Signature

**3**

**Chapter 1**

**1. Introduction**

with and without anaemia.

Introductory Chapter:

organs of the body including the cardiovascular system.

**2. Anaemia and iron deficiency in heart failure**

Heart Failure

Anaemia and Iron Deficiency in

The condition of an erythrocyte could be able to affect the internal and external conditions of all the vital and non-vital organs of a human body. These little biconcave disk-shaped red structures of approximately 8 μm in diameter and of about 2.5 μm in thickness can reflect the extent and type of parasitic, bacterial, and viral infections such as malaria, diarrhoea, and covid 19. Lack of enough healthy red blood cells to carry oxygen results in anaemia. Anaemia is a condition that occurs due to reduced haemoglobin (Hb) in the blood. Thus, the oxygencarrying capacity of the blood is reduced. When the oxygen-carrying capacity is reduced, the heart must work harder and faster to deliver the required oxygen to the body. If unrecognised, this process could result in serious damage to various

Commonly encountered symptoms of anaemia are generalised weakness, fatigue, pale appearance, shortness of breath, irritable mood, lack of concentration etc. However, if gone untreated, anaemia could result in, precipitate, or aggravate heart failure (HF). It could also result in arrhythmias & precipitate heart attacks (type 2 myocardial infarction). Anaemia is usually caused by inefficient production of red blood cells or the haemoglobin within these cells; by the loss of blood due to haemolysis within the circulation or bleeding issues; or due to other chronic medical conditions like kidney disease or cancer. However, the most common reason for anaemia remains iron deficiency (ID) which is critical to produce Hb. ID could exist

Anaemia & ID are common in patients with heart failure. They are associated with poor clinical status and worse prognosis [1]. Compared to a 10% prevalence of anaemia in the general population it is found in 30% of patients with stable heart failure and 50% in those hospitalised, inclusive of heart failure with reduce ejection fraction (HFrEF) or heart failure with preserved ejection fraction (HFpEF) [2–4]. Although the pathogenesis of anaemia in heart failure is multifactorial including deficiency of vitamin B12 & folate, low erythropoietin production due to renal involvement in heart failure, inflammatory components suppressing the production

In heart failure it is the ID rather than anaemia that serves as the predictor for clinical outcome [8]. impaired quality of life (QoL), reduced exercise capacity,

of red blood cells and Hb, ID remains one of the major contributors [4–7].

*Kaneez Fatima Shad and Nazar Luqman Bilgrami*
